bluuebunny/crossref_metadata_2025_split huggingface dataset:
Copeptin and risk stratification in patients with acute dyspnea
Authors: Potocki Mihael , Breidthardt Tobias , Mueller Alexandra , Reichlin Tobias , Socrates Thenral , Arenja Nisha , Reiter Miriam , Morgenthaler Nils G , Bergmann Andreas , Noveanu Markus , Buser Peter T , Mueller Christian 
Published: November 2010

Abstract
Introduction
The identification of patients at highest risk for adverse outcome who are presenting with acute dyspnea to the emergency department remains a challenge. This study investigates the prognostic value of Copeptin, the C-terminal part of the vasopressin prohormone alone and combined to N-terminal pro B-type natriuretic peptide (NT-proBNP) in patients with acute dyspnea.

Methods
We conducted a prospective, observational cohort study in the emergency department of a university hospital and enrolled 287 patients with acute dyspnea.

Results
Copeptin levels were elevated in non-survivors (n = 29) compared to survivors at 30 days (108 pmol/l, interquartile range (IQR) 37 to 197 pmol/l) vs. 18 pmol/l, IQR 7 to 43 pmol/l; P < 0.0001). The areas under the receiver operating characteristic curve (AUC) to predict 30-day mortality were 0.83 (95% confidence interval (CI) 0.76 to 0.90), 0.76 (95% CI 0.67 to 0.84) and 0.63 (95% CI 0.53 to 0.74) for Copeptin, NT-proBNP and BNP, respectively (Copeptin vs. NTproBNP P = 0.21; Copeptin vs. BNP P = 0.002). When adjusted for common cardiovascular risk factors and NT-proBNP, Copeptin was the strongest independent predictor for short-term mortality in all patients (HR 3.88 (1.94 to 7.77); P < 0.001) and especially in patients with acute decompensated heart failure (ADHF) (HR 5.99 (2.55 to 14.07); P < 0.0001). With the inclusion of Copeptin to the adjusted model including NTproBNP, the net reclassification improvement (NRI) was 0.37 (P < 0.001). An additional 30% of those who experienced events were reclassified as high risk, and an additional 26% without events were reclassified as low risk.

Conclusions
Copeptin is a new promising prognostic marker for short-term mortality independently and additive to natriuretic peptide levels in patients with acute dyspnea.
High-sensitivity troponin T as a marker of myocardial injury after radiofrequency catheter ablation
Authors: Vasatova M , Pudil R , Tichy M , Buchler T , Horacek J M , Haman L , Parizek P , Palicka V 
Published: November 2010

Background The aim of our study was to monitor radiofrequency catheter ablation-induced myocardial damage by measuring high-sensitivity cardiac troponin T (hs-cTnT). Methods Serum concentrations of hs-cTnT (Elecsys 2010 system, Roche) were measured in 73 healthy blood donors and serially in 27 patients who had samples taken both before and 24 h after radiofrequency ablation (RFA) for atrioventricular nodal re-entry tachycardia (AVNRT), atrial fibrillation (AF) or right atrial flutter (AFL). Results Significant increases of hs-cTnT were seen in patients after RFA (AVNRT: P = 0.0115, AF: P = 0.0011, AFL: P = 0.0009). Postprocedural serum hs-cTnT correlated with the number of radiofrequency applications and with the duration of RFA procedure. Spearman's coefficient of rank correlation ( r) were as follows: hs-cTnT versus RFA duration: r = 0.771 ( P < 0.001); hs-cTnT versus number of pulses: r = 0.708 ( P < 0.001). Patients with the diagnosis of AVNRT had lower serum hs-cTnT concentration after RFA compared with AFL ( P < 0.0001) and AF ( P < 0.0001) patients. Conclusions Our data indicate that RFA causes a significant increase of serum hs-cTnT concentration that could be used to monitor myocardial injury.
Plerixafor Dosing and Administration in a Patient with Dialysis-Dependent Renal Failure
Authors: Gregory Kelly M , Rao Kamakshi V , Armistead Paul M 
Published: November 2010

Objective: To report on the use of plerixafor in a patient with multiple myeloma and dialysis-dependent renal failure. Case Summary: A 38-year-old man with multiple myeloma and dialysis-dependent renal failure was evaluated for stem cell transplantation. Stem cell mobilization with 6 doses of granulocyte colony-stimulating factor (G-CSF) 10 μg/kg/day yielded an inadequate maximum pre-apheresis CD34+ count of 5.6 cells/μL. The patient was treated with a postdialysis subcutaneous dose of plerixafor 160 μg/kg after 4 days of G-CSF therapy. After a single dose of plerixafor, the patient's pre-apheresis CD34+ count was 125.6 cells/μL. After 1 apheresis session, the stem cell collection yield was 5.33 × 105 CD34+ cells/kg. There were no observed plerixafor toxicities. The patient underwent successful autologous stem cell transplantation. Times to neutrophil and platelet engraftment were 12 and 15 days, respectively. At 100-day follow-up, the patient's myeloma was in remission and he met all criteria for durable engraftment. Discussion: Renal impairment is a common comorbidity in patients with multiple myeloma. Plerixafor is a chemokine receptor 4 antagonist approved for use to mobilize stem cells for collection and subsequent autologous transplantation in patients with non-Hodgkin's lymphoma and multiple myeloma. To date, there is limited information on safe and effective dosing and administration of plerixafor in patients who are dialysis-dependent. This report describes the use of plerixafor in a patient with multiple myeloma and dialysis-dependent renal failure. Conclusions: Based on our experience, we are instituting a policy to administer plerixafor at Food and Drug Administration–approved renal adjustment doses in patients on hemodialysis, with dialysis sessions scheduled prior to plerixafor administration and repeated as necessary after apheresis and prior to subsequent plerixafor doses. If clinically feasible, dialysis should be held during the days required to collect stem cells.
Antibiotic Prophylaxis for Prevention of Spontaneous Bacterial Peritonitis in Patients Without Gastrointestinal Bleeding
Authors: Segarra-Newnham Marisel , Henneman Amy 
Published: November 2010

Objective: To review relevant studies for both primary and secondary antibiotic prophylaxis of spontaneous bacterial peritonitis (SBP) in patients with cirrhosis without gastrointestinal bleeding. Data Sources: A search of PubMed (1980-July 2010) was conducted using the terms prophylaxis, SBP, and antibiotics. A manual review of bibliographies was conducted for inclusion of relevant articles. Study Selection and Data Extraction: Prospective studies and meta-analyses published in English were included. Data Synthesis: Ten trials and 3 meta-analyses were included. Of the 10 trials, 2 examined the use of secondary prophylaxis for prevention of subsequent episodes of SBP, 4 examined the use of primary prophylaxis to prevent an initial SBP episode, and 4 examined the use of antibiotic prophylaxis in a mixed population. Seven trials evaluated the use of an antibiotic compared to placebo or no treatment. Only 1 trial evaluated norfloxacin versus trimethoprim/sulfamethoxazole. Trial duration varied from 24 days to 12 months. In general, trials examining norfloxacin as secondary prophylaxis found significantly decreased occurrence of SBP but no significant difference in mortality rates. Primary prophylaxis studies found no significant difference in the incidence of infections, including SBP, with norfloxacin or ciprofloxacin treatment but significantly lower incidence of gram-negative infections. Mixed population studies found a significantly decreased incidence of SBP but no significant difference in mortality. In the 3 meta-analyses, a significant decrease in mortality and an overall decrease in SBP incidence in the treatment groups were noted. Conclusions: Based on currently available data, the use of prophylactic antibiotic therapy is warranted for the prevention of recurrent SBP in patients with cirrhosis and ascites. In patients with low ascetic fluid protein and at least 1 more risk factor, primary prophylaxis may be considered. Further studies with improved methodology are needed to determine whether prophylactic antibiotic therapy has an impact on mortality.
Cardiology: Pharmacologic Management of Heart Failure with Preserved Ejection Fraction
Authors: Huang Dana , Cheng Judy WM 
Published: November 2010

Objective: To provide an overview of heart failure with preserved ejection fraction (HFPEF), as well as its pathophysiology, diagnosis, and clinical evidence regarding its pharmacologic management. Data Sources: Peer-reviewed articles were identified from MEDLINE, International Pharmaceutical Abstracts, and Current Contents (all 1966-August 2010) using the search terms heart failure with preserved ejection fraction, diastolic dysfunction, diastolic heart failure, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), digoxin, β-blockers, calcium-channel blockers, and vasodilators. Citations from available articles were also reviewed for additional references. Study Selection and Data Extraction: Fourteen published manuscripts relating to pharmacologic management of HFPEF were identified. Data Synthesis: The prevalence of HFPEF has continued to increase. Compared to heart failure with left ventricular systolic dysfunction, HFPEF has been largely understudied. Unlike in the management of heart failure with left ventricular systolic dysfunction, ACE inhibitors, ARBs, β-blockers, and aldosterone antagonists did not demonstrate mortality benefit in HFPEF, with the exception of one small study evaluating the use of propranolol. However, this study enrolled a small number of patients with recent history of myocardial infarction, which limited the generalizability of the results. Most of the current evidence centers on morbidity benefits and symptom reduction. One study showed that treatment with candesartan reduced hospital admissions in this population of patients. Management of HFPEF still focuses on optimally managing underlying diseases (eg, hypertension). Conclusions: Much remains to be learned about the appropriate pharmacologic management of patients with HFPEF. Hypertension is in most cases the predominant contributor to its development and progression. For this reason, antihypertensive treatment, including ACE inhibitors, ARBs, β-blockers, and calcium-channel blockers, has been evaluated and is recommended to control the disease in this patient population, although these agents have not demonstrated significant benefit beyond blood pressure control. Further research into the pathophysiology of HFPEF may contribute to identifying the most optimal agent in managing this disease.
Subcutaneous Unfractionated Heparin for Treatment of Venous Thromboembolism in End-Stage Renal Disease
Authors: Metzger Nicole L , Chesson Melissa M 
Published: November 2010

Objective: To report 3 cases of venous thromboembolism (VTE) in patients with end-stage renal disease (ESRD) treated with subcutaneous unfractionated heparin (UFH) bridged with warfarin. Case Summaries: Three patients with ESRD were successfully treated for VTE with unmonitored, fixed-dose subcutaneous UFH every 12 hours and doseadjusted warfarin. The first patient was initiated on continuous infusion UFH for deep-vein thrombosis, but due to poor vascular access, nurses were unable to consistently measure anti-Xa levels. Therefore, subcutaneous UFH 17,500 units (~245 units/kg/dose) every 12 hours was initiated. Oral warfarin 5 mg/day was started the following day. The patient received 4 days of inpatient subcutaneous UFH and then was discharged to complete the bridge as an outpatient. The second patient received subcutaneous UFH 10,000 units (~244 units/kg/dose) every 12 hours and oral warfarin 2.5 mg/day to treat a nonocclusive thrombus along her right femoral vein hemodialysis catheter. The patient received 1 day of inpatient subcutaneous UFH treatment prior to discharge and continued bridge therapy with warfarin as an outpatient. The third patient was initiated on subcutaneous UFH 20,000 units (~223 units/kg/dose) every 12 hours and oral warfarin 7.5 mg/day due to a subtherapeutic INR (1.50) 5 days after receiving fresh frozen plasma to reduce her therapeutic INR for a procedure. The patient received 2 doses of subcutaneous UFH as an inpatient before treatment was discontinued because her INR was therapeutic at 2.3. Discussion: Subcutaneous UFH has been used to treat VTE since the early 1980s; however, with the advent of low-molecular-weight heparin (LMWH), subcutaneous UFH use diminished. Several studies comparing the use of subcutaneous UFH to both continuous infusion UFH and LMWH concluded that subcutaneous UFH is a safe and efficacious alternative. The 2008 Chest Guidelines for Antithrombotic Therapy for Venous Thromboembolic Disease support the use of subcutaneous UFH for the treatment of VTE with a Grade 1A recommendation and provide a Grade 2C recommendation for use of UFH over LMWH for patients with VTE and severe renal failure. Conclusions: Safe and convenient treatment options for VTE in patients with ESRD are limited. Fixed-dose, unmonitored subcutaneous UFH as a bridge to warfarin therapy is an effective option in patients with ESRD and those with financial restrictions. The pharmacist plays a key role in identifying patients for whom subcutaneous UFH treatment may be a viable alternative, recommending an appropriate dosing regimen, and educating health-care professionals and patients about safe use.
Appetite-regulating hormones cortisol and peptide YY are associated with disordered eating psychopathology, independent of body mass index
Authors: Lawson Elizabeth A , Eddy Kamryn T , Donoho Daniel , Misra Madhusmita , Miller Karen K , Meenaghan Erinne , Lydecker Janet , Herzog David , Klibanski Anne 
Published: November 2010

ObjectiveDisordered eating occurs in women at both weight extremes of anorexia nervosa (AN) and obesity. Cortisol, peptide YY (PYY), leptin, and ghrelin are hormones involved in appetite and feeding behavior that vary with weight and body fat. Abnormal levels of these hormones have been reported in women with AN, functional hypothalamic amenorrhea (HA), and obesity. The relationship between appetite-regulating hormones and disordered eating psychopathology is unknown. We therefore studied the relationship between orexigenic and anorexigenic hormones and disordered eating psychopathology in women across a range of weights.DesignA cross-sectional study of 65 women, 18–45 years: 16 with AN, 12 normal-weight with HA, 17 overweight or obese, and 20 normal-weight in good health.MethodsTwo validated measures of disordered eating psychopathology, the Eating Disorders Examination-Questionnaire (EDE-Q) and Eating Disorders Inventory-2 (EDI-2), were administered. Fasting PYY, leptin, and ghrelin levels were measured; cortisol levels were pooled from serum samples obtained every 20 min from 2000 to 0800 h.ResultsCortisol and PYY levels were positively associated with disordered eating psychopathology including restraint, eating concerns, and body image disturbance, independent of body mass index (BMI). Although leptin levels were negatively associated with disordered eating psychopathology, these relationships were not significant after controlling for BMI. Ghrelin levels were generally not associated with EDE-Q or EDI-2 scores.ConclusionsHigher levels of cortisol and PYY are associated with disordered eating psychopathology independent of BMI in women across the weight spectrum, suggesting that abnormalities in appetite regulation may be associated with specific eating disorder pathologies.
Pregnancy in women heterozygous for MCT8 mutations: risk of maternal hypothyroxinemia and fetal care
Authors: Ramos Helton Estrela , Morandini Melina , Carré Aurore , Tron Elodie , Floch Corinne , Mandelbrot Laurent , Neri Nathalie , De Sarcus Benoit , Simon Albane , Bonnefont Jean Paul , Amiel Jeanne , Desguerre Isabelle , Valayannopoulos Vassili , Castanet Mireille , Polak Michel 
Published: November 2010

ContextMonocarboxylate transporter 8 (MCT8 or SLC16A2) mutations cause X-linked Allan–Herndon–Dudley syndrome. Heterozygous females are usually asymptomatic, but pregnancy may modify thyroid function and MCT8 is expressed in the placenta, suggesting that maternal and fetal abnormalities might develop even in the absence of MCT8 fetal mutation. Genetic counseling is so far based on X-linked transmission, and prenatal diagnosis is rarely performed.ObjectiveTo describe thyroid function and the prenatal diagnosis in pregnant mothers harboring heterozygous MCT8 mutations and management of the persistent maternal hypothyroxinemia.PatientsTwo women heterozygous for MCT8 mutations (c.1690G>A and c.1393-1G>C) were monitored throughout pregnancy.MethodsPrenatal diagnosis included sex determination, direct MCT8 sequencing, and familial linkage analysis. Ultrasonography and hormonal assays for maternal thyroid function evaluation were performed serially during pregnancy. Neonatal thyroid hormonal status was assessed.ResultsNone of the three fetuses (two males and one female) carried MCT8 mutations. One of the two heterozygous mothers revealed gestational hypothyroxinemia, prompting early levothyroxine (l-T4) therapy until delivery. The second heterozygous mother showed normal thyroid function but was preventively traited by l-T4 and all of the three neonates had normal thyroid hormone levels and thyroid gland at birth, suggesting advantages of prenatal care and/or compensatory mechanisms.ConclusionHeterozygous MCT8 women should be monitored for requirement of l-T4 therapy to prevent fetal and neonatal hypothyroidism and to avoid risk of potential cognitive delay due to gestational hypothyroxinemia. Moreover, when the disease-causing mutation is known and/or the first child is affected, prenatal diagnosis for male fetuses should be assessed early for MCT8 mutations by direct sequencing.
The Putative Lipid Transporter, Arv1, Is Required for Activating Pheromone-Induced MAP Kinase Signaling in Saccharomyces cerevisiae
Authors: Villasmil Michelle L , Ansbach Alison , Nickels Joseph T 
Published: November 2010

Abstract
Saccharomyces cerevisiae haploid cells respond to extrinsic mating signals by forming polarized projections (shmoos), which are necessary for conjugation. We have examined the role of the putative lipid transporter, Arv1, in yeast mating, particularly the conserved Arv1 homology domain (AHD) within Arv1 and its role in this process. Previously it was shown that arv1 cells harbor defects in sphingolipid and glycosylphosphatidylinositol (GPI) biosyntheses and may harbor sterol trafficking defects. Here we demonstrate that arv1 cells are mating defective and cannot form shmoos. They lack the ability to initiate pheromone-induced G1 cell cycle arrest, due to failure to polarize PI(4,5)P2 and the Ste5 scaffold, which results in weakened MAP kinase signaling activity. A mutant Ste5, Ste5Q59L, which binds more tightly to the plasma membrane, suppresses the MAP kinase signaling defects of arv1 cells. Filipin staining shows arv1 cells contain altered levels of various sterol microdomains that persist throughout the mating process. Data suggest that the sterol trafficking defects of arv1 affect PI(4,5)P2 polarization, which causes a mislocalization of Ste5, resulting in defective MAP kinase signaling and the inability to mate. Importantly, our studies show that the AHD of Arv1 is required for mating, pheromone-induced G1 cell cycle arrest, and for sterol trafficking.
Genetic Evidence for Antagonism Between Pak Protein Kinase and Rho1 Small GTPase Signaling in Regulation of the Actin Cytoskeleton During Drosophila Oogenesis
Authors: Vlachos Stephanie , Harden Nicholas 
Published: November 2010

Abstract
During Drosophila oogenesis, basally localized F-actin bundles in the follicle cells covering the egg chamber drive its elongation along the anterior–posterior axis. The basal F-actin of the follicle cell is an attractive system for the genetic analysis of the regulation of the actin cytoskeleton, and results obtained in this system are likely to be broadly applicable in understanding tissue remodeling. Mutations in a number of genes, including that encoding the p21-activated kinase Pak, have been shown to disrupt organization of the basal F-actin and in turn affect egg chamber elongation. pak mutant egg chambers have disorganized F-actin distribution and remain spherical due to a failure to elongate. In a genetic screen to identify modifiers of the pak rounded egg chamber phenotype several second chromosome deficiencies were identified as suppressors. One suppressing deficiency removes the rho1 locus, and we determined using several rho1 alleles that removal of a single copy of rho1 can suppress the pak phenotype. Reduction of any component of the Rho1-activated actomyosin contractility pathway suppresses pak oogenesis defects, suggesting that Pak counteracts Rho1 signaling. There is ectopic myosin light chain phosphorylation in pak mutant follicle cell clones in elongating egg chambers, probably due at least in part to mislocalization of RhoGEF2, an activator of the Rho1 pathway. In early egg chambers, pak mutant follicle cells have reduced levels of myosin phosphorylation and we conclude that Pak both promotes and restricts myosin light chain phosphorylation in a temporally distinct manner during oogenesis.
Validation of the Dutch Registry of Common Oral Clefts: Quality of Recording Specific Oral Cleft Features
Authors: Rozendaal Anna M. , Luijsterburg Antonius J.M. , Mohangoo Ashna D. , Ongkosuwito Edwin M. , De Vries Esther , Vermeij-Keers Christl 
Published: November 2010

Objective Since 1997, common oral clefts in the Netherlands have been recorded in the national oral cleft registry using a unique descriptive recording system. This study validates data on the topographic-anatomical structure, morphology, and side of individual anomalies of the primary palate and secondary palate that form the oral cleft. Design Validation study. Setting All 15 Dutch cleft palate teams reporting presurgery oral cleft patients to the national registry. Patients A random sample of 250 cases registered in the national database with oral clefts from 1997 through 2003; of these, 13 cases were excluded. Main Outcome Measures By linking registry data with clinical data, we identified differential recording rates by comparing the prevalence, and we measured the degree of agreement by computing validity and reliability statistics. Results The topographic-anatomical structures (lip, alveolus, and hard and soft palates) of the anomalies had near-perfect interdatabase agreement with a sensitivity of 88% to 99%. However, when analyzing the individual anomalies in detail (morphology and side), validity decreased and depended on morphological severity. This association was most evident for anomalies of the secondary palate. For example, sensitivity was higher for “complete cleft hard palate” (92%) than for “submucous cleft hard/soft palate” (69%). Conclusions Overall, the validity of Dutch registry data on oral clefts is good, supporting the feasibility of this unique recording system. However, when analyzing oral cleft data in detail, the quality appears to be related to anatomical location and morphological severity. This might have implications for etiologic research based on registry data and for guidelines on neonatal examination.