bluuebunny/crossref_metadata_2025_split huggingface dataset:
Delay in the Diagnosis of Acute Myocardial Infarction: Effect on Quality of Care and Its Assessment
Authors: Graff Louis G. , Wang Yun , Borkowski Brian , Tuozzo Kathy , Foody JoAnne M. , Krumholz Harlan M. , Radford Martha J. 
Published: August 2006

Abstract
Background:
Delay in diagnosis of acute myocardial infarction (AMI) may affect quality of care and its assessment.
Objectives:
To examine over time the frequency of delay in AMI diagnosis and the effect of this delay on the quality of patient care and its assessment.
Methods:
The authors examined the trend in coded admission diagnosis, age, comorbidities, procedures during hospitalization, and discharge status for 42,406 Connecticut Medicare cases with the principal discharge diagnosis of AMI for the time period 1992 through 2001. For 2,583 cases discharged in 1992 and 1993 and for 1,398 cases discharged in 1998 through 2001, the rates of administration of aspirin (ASA) and beta blocker (BB) on admission and discharge, by admission diagnosis, were ascertained.
Results:
For patients discharged with the principal diagnosis of AMI over the decade examined, the proportion with this diagnosis on admission fell (59% to 40%, p < 0.001), the proportion with a non–acute coronary syndrome (ACS) admission diagnosis rose (18% to 26%, p < 0.001), and the population aged (proportion older than 85 years of age increased from 16% to 28%, p < 0.001). Patients with ACS as the admission diagnosis more frequently received cardiac catheterization (during 2000–2001, 39% versus 17%, p < 0.001), percutaneous coronary intervention (19% versus 4%, p < 0.001), and evidence‐based therapy; during 1998–2001, opportunities to give ASA or BB on admission were fulfilled for 88% versus 73% (p < 0.001), and on discharge, for 87% versus 74% (p < 0.005).
Conclusions:
The diagnosis of AMI is delayed after admission for a significant proportion of cases who receive care that is measured to be of lower quality. There is a need to more effectively diagnose and treat these cases with delayed diagnosis and to develop new quality measures to address changes in the characteristics of patients who are hospitalized with AMI.
Emergency Department Sexually Transmitted Disease and Human Immunodeficiency Virus Screening: Findings from a National Survey
Authors: Gift Thomas L. , Hogben Matthew 
Published: August 2006

Abstract
Objectives:
To use a previously conducted national physician survey to determine the extent of human immunodeficiency virus (HIV) and sexually transmitted disease (STD) screening by emergency physicians compared with physicians practicing in other settings (primary care offices, hospital ambulatory care clinics, or other).
Methods:
From the survey responses, the authors determined the percentage of emergency physicians and physicians not practicing in EDs screening various patient groups for syphilis, gonorrhea, chlamydia, and HIV. Additional data from the survey (for practice location, physician gender, and patient demographics of race and gender) were used in multivariate logistic regressions to determine adjusted odds ratios (ORs).
Results:
Of 3,838 survey respondents providing answers to all questions analyzed for this study, 401 (10.5%) practiced in an emergency department. Of the remaining 3,437 physicians, 89% practiced in primary care offices or hospital ambulatory care clinics. Based on unadjusted ORs, emergency physicians were less likely than physicians not practicing in EDs to screen for all STDs and HIV in all patient groups (men, nonpregnant women, and pregnant women), although the differences in screening rates in male patients for chlamydia or gonorrhea were not significant. The adjusted ORs varied from 0.136 (for HIV screening of pregnant women) to 1.177 (for gonorrhea screening of pregnant women). All adjusted ORs that were significant at p < 0.05 were < 1.0.
Conclusions:
Although prior research has shown that STD and HIV rates are relatively high in emergency department patients compared with the population as a whole, screening rates are lower than in other settings. Addressing barriers may increase screening rates.
A Comparison of Five Simplified Scales to the Out‐of‐hospital Glasgow Coma Scale for the Prediction of Traumatic Brain Injury Outcomes
Authors: Gill Michelle , Steele Robert , Windemuth Ryan , Green Steven M. 
Published: August 2006

Abstract
Background:
The 15‐point Glasgow Coma Scale (GCS) frequently is used in the initial evaluation of traumatic brain injury (TBI) in out‐of‐hospital settings. We hypothesized that the GCS might be unnecessarily complex for out‐of‐hospital use.
Objectives:
To assess whether a simpler scoring system might demonstrate similar accuracy in the prediction of TBI outcomes.
Methods:
We performed a retrospective analysis of a trauma registry consisting of patients evaluated at our Level 1 trauma center from 1990 to 2002. The ability of out‐of‐hospital GCS scores to predict four clinically relevant TBI outcomes (emergency intubation, neurosurgical intervention, brain injury, and mortality) by using areas under receiver operating characteristic curves (AUROCs) was calculated. The same analyses for five simplified scales were performed, and compared with the predictive accuracies of the total GCS score.
Results:
In this evaluation of 7,233 trauma patients over a 12‐year period of time, the AUROCs for the total GCS score were 0.83 (95% confidence interval [CI] = 0.81 to 0.84) for emergency intubation, 0.86 (95% CI = 0.85 to 0.88) for neurosurgical intervention, 0.83 (95% CI = 0.82 to 0.84) for brain injury, and 0.89 (95% CI = 0.88 to 0.90) for mortality. The five simplified scales approached the performance of the total GCS score for all clinical outcomes.
Conclusions:
In the evaluation of injured patients, five simplified neurological scales approached the performance of the total GCS score for the prediction of four clinically relevant TBI outcomes.
Lethal congenital contracture syndrome (LCCS) and other lethal arthrogryposes in Finland—An epidemiological study
Authors: Pakkasjärvi Niklas , Ritvanen Annukka , Herva Riitta , Peltonen Leena , Kestilä Marjo , Ignatius Jaakko 
Published: August 2006

AbstractArthrogryposis multiplex congenita is a heterogeneous group of disorders characterized by multiple contractures with an estimated frequency of 1 in 3,000 births. With improving diagnostic methods, increasing numbers of fetuses with arthrogryposis are found. The pathogenetic mechanisms are relatively well known but the epidemiology and genetics of the prenatally lethal forms of arthrogryposis are less well known. In this study we collected all cases of a multiple contractures diagnosed in Finland during 1987–2002 including live born infants, stillbirths, and terminated pregnancies. Ninety‐two cases of 214 suffered intrauterine demise (68 selective pregnancy terminations and 24 stillbirths) and 58 died in infancy. In 141 out of these cases the diagnosis could be included within lethal arthrogryposes, with a prevalence of 1 in 6,985 (1.43/10,000) births. Of these, 59 had spinal cord pathology at autopsy and thus were of neurogenic origin. Thirty‐nine cases had lethal congenital contracture syndrome (LCCS) clinically characterized by total immobility of the fetus at all ultrasound examinations (12 weeks or later), multiple joint contractures in both upper and lower limbs, hydrops, and fetal death before the 32nd week of pregnancy. LCCS is noted as a unique Finnish disorder with a prevalence of 1 in 25,250 (0.40/10,000) births and is a major cause of lethal arthrogryposis in Finland. © 2006 Wiley‐Liss, Inc.
SALL1 mutations in sporadic Townes–Brocks syndrome are of predominantly paternal origin without obvious paternal age effect
Authors: Böhm Johann , Munk‐Schulenburg Susanne , Felscher Stephanie , Kohlhase Jürgen 
Published: August 2006

AbstractAutosomal dominant Townes–Brocks syndrome (TBS) is characterized by imperforate anus, triphalangeal and supernumerary thumbs, dysplastic ears and sensorineural hearing loss, and may also involve other organ systems. Strong inter‐ and intrafamiliar variability is known. Approximately 50% of TBS cases are sporadic and due to de novo mutations in the SALL1 gene. SALL1 encodes a zinc finger protein operating as a transcriptional repressor and localizing to pericentromeric heterochromatin. We traced the parental origin of SALL1 mutations in sporadic TBS by analysis of linkage between SALL1 mutations and exonic or intronic polymorphisms in 16 families with 10 different mutations. Mutations were of paternal origin in 14 of 16 cases (87.5%). Paternal origin was independent of the mutation type. The mean paternal age at conception was 29.9 and the mean maternal age 26.5 years. We conclude that de novo mutations in SALL1 mostly occur on the paternally derived chromosome 16 without an obvious age effect. © 2006 Wiley‐Liss, Inc.
Clinical outcome of infants with confined placental mosaicism and intrauterine growth restriction of unknown cause
Authors: Miura Kiyonori , Yoshiura Koh‐ichiro , Miura Shoko , Kondoh Tatsuro , Harada Naoki , Yamasaki Kentaro , Fujimoto Yoko , Yamasaki Yoko , Tanigawa Terumi , Kitajima Yuriko , Shimada Takako , Yoshida Atsushi , Nakayama Daisuke , Tagawa Masato , Yoshimura Shuichiro , Wagstaff Joseph , Jinno Yoshihiro , Ishimaru Tadayuki , Niikawa Norio , Masuzaki Hideaki 
Published: August 2006

AbstractThe purpose of this study was to know a role of confined placental mosaicism (CPM) in perinatal outcome and postnatal growth and development of infants with intrauterine growth restriction (IUGR). We selected 50 infants with IUGR (<−2.0 SD) from 3,257 deliveries in a regional medical center during the past 10‐year period, and carried out cytogenetic and molecular analyses in their placenta and cord blood. Of the 50 infants, 8 had CPM (CPM group) and were composed of five single (CPM2, 7, 13, 22, and 22), one double (CPM7/13), and one quadruple trisomy (CPM2/7/15/20), and one partial monosomy [del(2)(p16)]. The origin of an extra chromosome of trisomy was maternal in six cases of CPM, paternal in one, and undetermined in one. Uniparental disomy in disomic cell lines was ruled out in all these mosaics. We also compared clinical parameters for perinatal outcome between CPM group and infants without evidence of CPM (non‐CPM group), such as maternal and gestational age, birth weight, Apgar score, cord blood pH, gender, and uterine artery patterns by Doppler ultrasonography, as well as weight, height, and developmental quotient (DQ) by Denver Developmental Screening Test at age 12 months. Phenotypic abnormalities were noted in two infants with CPM and three infants of non‐CPM group: One with CPM22 had ASD and hypospadias, one with CPM7/13 had Russell–Silver syndrome (RSS), and one without CPM had polydactyly, and two without CPM had RSS. All but one infant with CPM are alive at age 12 months. Among the clinical parameters, the detection rate of a notch waveform pattern of the uterine artery was significantly higher in the CPM group (P < 0.05). However, no significant difference was noted in perinatal outcome of pregnancy and in DQ at age 12 months between the two groups. Interestingly, short stature (<−2 SD) at age 12 months was more frequently seen in CPM group (7/8 infants with CPM vs. 8/15 infants without CPM), although no statistically significant difference was obtained. The information obtained will be useful for perinatal care and genetic counseling for infants with IUGR and CPM. © 2006 Wiley‐Liss, Inc.
Increased eNOS accounts for changes in connexin expression in renal arterioles during diabetes
Authors: Zhang Jian Hong , Kawashima Seinosuke , Yokoyama Mitsuhiro , Huang Paul , Hill Caryl E. 
Published: August 2006

AbstractPrevious studies have shown that connexin (Cx) expression is considerably higher in the preglomerular compared to postglomerular vasculature and that these differences are accentuated during diabetes. Since nitric oxide (NO) has been reported to alter Cx expression in endothelial cells and muscle cells and NO bioavailability is altered in diabetes, we hypothesized that NO may be responsible for the changes during diabetes. Cx expression was studied using immunohistochemistry in mice in which eNOS expression was either upregulated (eNOS transgenic) or downregulated (eNOS knockout). Diabetes was induced intraperitoneally with a single dose of alloxan or multiple low doses of streptozotocin. Expression of Cx40 in smooth muscle cells of afferent arterioles was increased, while expression of Cx43 in endothelial cells of efferent arterioles was absent in eNOS transgenic mice, similar to the changes occurring in wild‐type mice during diabetes. Expression of Cx40 and Cx43 in eNOS knockout mice was not different from control; however, induction of diabetes in eNOS knockout mice failed to produce any changes in Cx40 or Cx43 in either afferent or efferent arterioles. Immunohistochemistry showed that eNOS expression was increased in the endothelium of renal arterioles in wild‐type diabetic and eNOS transgenic mice, but absent from arterioles of eNOS knockout mice. We conclude that changes occurring in Cx expression in afferent and efferent arterioles during diabetes may result from increased eNOS. Anat Rec Part A, 288A:1000–1008, 2006. © 2006 Wiley‐Liss, Inc.
Plan to be Flexible: A Commentary on Adaptive Designs
Authors: Shih Weichung Joe 
Published: August 2006

AbstractThis is a discussion of the following three papers appearing in this special issue on adaptive designs: ‘Nested repeated confidence intervals and switching between noninferiority and superiority’ by Joachim Hartung and Guido Knapp; ‘Confirmatory Seamless Phase II/III Clinical trials with Hypotheses Selection at Interim: General Concepts’ by Frank Bretz, Heinz Schmidli, Franz König, Amy Racine and Willi Maurer; and ‘Confirmatory Seamless Phase II/III Clinical Trials with Hypotheses Selection at Interim: Applications and Practical Considerations’ by Heinz Schmidli, Frank Bretz, Amy Racine and Willi Maurer. (© 2006 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Discrimination of normal, benign, and malignant breast tissues by Raman spectroscopy
Authors: Chowdary M. V. P. , Kumar K. Kalyan , Kurien Jacob , Mathew Stanley , Krishna C. Murali 
Published: August 2006

AbstractBreast cancers are the leading cancers among females. Diagnosis by fine needle aspiration cytology (FNAC) is the gold standard. The widely practiced screening method, mammography, suffers from high false positive results and repeated exposure to harmful ionizing radiation. As with all other cancers survival rates are shown to heavily depend on stage of the cancers (Stage 0, 95%; Stage IV, 75%). Hence development of more reliable screening and diagnosis methodology is of considerable interest in breast cancer management. Raman spectra of normal, benign, and malignant breast tissue show significant differences. Spectral differences between normal and diseased breast tissues are more pronounced than between the two pathological conditions, malignant and benign tissues. Based on spectral profiles, the presence of lipids (1078, 1267, 1301, 1440, 1654, 1746 cm−1) is indicated in normal tissue and proteins (stronger amide I, red shifted ΔCH2, broad and strong amide III, 1002, 1033, 1530, 1556 cm−1) are found in benign and malignant tissues. The major differences between benign and malignant tissue spectra are malignant tissues seem to have an excess of lipids (1082, 1301, 1440 cm−1) and presence of excess proteins (amide I, amide III, red shifted ΔCH2, 1033, 1002 cm−1) is indicated in benign spectra. The multivariate statistical tool, principal components analysis (PCA) is employed for developing discrimination methods. A score of factor 1 provided a reasonable classification of all three tissue types. The analysis is further finetuned by employing Mahalanobis distance and spectral residuals as discriminating parameters. This approach is tested both retrospectively and prospectively. The limit test, which provides the most unambiguous discrimination, is also considered and this approach clearly discriminated all three tissue types. These results further support the efficacy of Raman spectroscopic methods in discriminating normal and diseased breast tissues. © 2006 Wiley Periodicals, Inc. Biopolymers 83:556–569, 2006This article was originally published online as an accepted preprint. The “Published Online” date corresponds to the preprint version. You can request a copy of the preprint by emailing the Biopolymers editorial office at biopolymers@wiley.com
Percutaneous ex‐vivo femoral arterial bypass: A novel approach for treatment of acute limb ischemia as a complication of femoral arterial catheterization
Authors: Merhi William M. , Turi Zoltan G. , Dixon Simon , Safian Robert D. 
Published: August 2006

AbstractThis report describes the use of a percutaneous ex‐vivo femoral arterial bypass in three patients with acute lower extremity ischemia that occurred as a complication of femoral artery catheterization. Utilizing standard equipment and techniques, a percutaneous ex‐vivo femoral artery bypass can restore antegrade flow to the ischemic limb in patients with impaired aorto‐iliac inflow circulation, which may arise from iatrogenic dissection or the need for large in‐dwelling sheaths required for hemodynamic support. This technique is considered a temporizing measure when conventional therapies are not possible. Contrast angiography is recommended to localize and define the cause of limb ischemia, and to permit safe placement of vascular sheaths in the “donor and recipient” arteries. © 2006 Wiley‐Liss, Inc.
Bacteroides fragilisenterotoxin induces cyclooxygenase‐2 and fluid secretion in intestinal epithelial cells through NF‐κB activation
Authors: Kim Jung Mogg , Lee Jin Young , Yoon Young Mee , Oh Yu‐Kyoung , Kang Ju Seop , Kim Yeong‐Jeon , Kim Kyoung‐Ho 
Published: August 2006

AbstractBacteroides fragilisproduces an approximately 20‐kDa heat‐labile toxin (B. fragilisenterotoxin, BFT) which is known to be associated with diarrhea. To determine whether cyclooxygenase (COX)‐2,viaNF‐κB activation, can contribute to BFT‐induced diarrhea, the relationship between COX‐2 expression and fluid secretion in BFT‐stimulated human intestinal epithelial cells was examined. BFT stimulation increased the expression of COX‐2, but not COX‐1, in human intestinal epithelial cells. Suppression of the NF‐κB signal significantly decreased COX‐2 expression in response to BFT stimulation. Prostaglandin E2(PGE2) levels were increased in parallel with COX‐2 expression, and, conversely, PGE2production was significantly inhibited when COX‐2 or NF‐κB activities were suppressed using COX‐2 small interfering RNA (siRNA), p65 NF‐κB subunit siRNA, or a retrovirus encoding the IκBα superrepressor. In addition, a selective COX‐2 inhibitor, NS‐398, significantly inhibited the increased cAMP level induced by BFT stimulation. Furthermore, a selective COX‐2 inhibitor prevented BFT‐induced PGE2production and ileal fluid secretion in a mouse ileal loop model. These results suggest that the secretory response to BFT stimulation may be mediated by the production of PGE2, through NF‐κB activation and the up‐regulation of COX‐2 in intestinal epithelial cells.
Chiral Half‐Sandwich Ruthenium(II) Complexes as Catalysts in 1,3‐Dipolar Cycloaddition Reactions of Nitrones with Methacrolein (Eur. J. Inorg. Chem. 16/2006)
Authors: Carmona Daniel , Lamata M. Pilar , Viguri Fernando , Ferrer Joaquina , García Néstor , Lahoz Fernando J. , Martín M. Luisa , Oro Luis A. 
Published: August 2006

AbstractThe cover picture shows the structure of a chiral half‐sandwich ruthenium(II) complex with the (4S)‐2‐[2‐(diphenylphosphanyl)phenyl]‐4‐isopropyl‐1,3‐oxazoline ligand that catalyzes the asymmetric 1,3‐dipolar cycloaddition reaction of nitrones with methacrolein. Catalyst precursors as well as dipolarophile or nitrone‐containing intermediates have been isolated and spectroscopically and/or crystallographically characterized. Details are discussed in the article by D. Carmona, M. P. Lamata, L. A. Oro et al. on p. 3155 ff.
Distinct patterns of DNA copy number alteration are associated with different clinicopathological features and gene‐expression subtypes of breast cancer
Authors: Bergamaschi Anna , Kim Young H. , Wang Pei , Sørlie Therese , Hernandez‐Boussard Tina , Lonning Per E. , Tibshirani Robert , Børresen‐Dale Anne‐Lise , Pollack Jonathan R. 
Published: August 2006

AbstractBreast cancer is a leading cause of cancer‐death among women, where the clinicopathological features of tumors are used to prognosticate and guide therapy. DNA copy number alterations (CNAs), which occur frequently in breast cancer and define key pathogenetic events, are also potentially useful prognostic or predictive factors. Here, we report a genome‐wide array‐based comparative genomic hybridization (array CGH) survey of CNAs in 89 breast tumors from a patient cohort with locally advanced disease. Statistical analysis links distinct cytoband loci harboring CNAs to specific clinicopathological parameters, including tumor grade, estrogen receptor status, presence of TP53 mutation, and overall survival. Notably, distinct spectra of CNAs also underlie the different subtypes of breast cancer recently defined by expression‐profiling, implying these subtypes develop along distinct genetic pathways. In addition, higher numbers of gains/losses are associated with the “basal‐like” tumor subtype, while high‐level DNA amplification is more frequent in “luminal‐B” subtype tumors, suggesting also that distinct mechanisms of genomic instability might underlie their pathogenesis. The identified CNAs may provide a basis for improved patient prognostication, as well as a starting point to define important genes to further our understanding of the pathobiology of breast cancer. This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/1045‐2257/suppmat. © 2006 Wiley‐Liss, Inc.
Hippocampal place cells: The “where” of episodic memory?
Authors: Kentros Clifford 
Published: August 2006

AbstractNeuropsychologists have clearly implicated the hippocampus in the consolidation of memory, particularly episodic memory, the mental replay of past experiences. When recorded from behaving animals, by far the most obvious firing pattern of the primary neurons of the hippocampus is the place field: a cell tends to fire only when the animal's head is in a particular part of its environment. It seems reasonable to suspect that the primary firing correlate of the primary neurons of a structure should underlie the primary function of that structure as revealed by behavioral lesion experiments. However, we are currently still at a loss to explain how the firing of hippocampal neurons contributes to hippocampal function. This review seeks to examine the commonalities between place cells and episodic memory, and posits that an analogy can be made between the stabilization of place fields and the consolidation of memory. © 2006 Wiley‐Liss, Inc.