bluuebunny/crossref_metadata_2025_split huggingface dataset:
Exploring Biological Relationships Between Calving Traits in Primiparous Cattle with a Bayesian Recursive Model
Authors: de Maturana Evangelina López , Wu Xiao-Lin , Gianola Daniel , Weigel Kent A , Rosa Guilherme J M 
Published: November 2008

Abstract
Structural equation models (SEMs) of a recursive type with heterogeneous structural coefficients were used to explore biological relationships between gestation length (GL), calving difficulty (CD), and perinatal mortality, also known as stillbirth (SB), in cattle, with the last two traits having categorical expression. An acyclic model was assumed, where recursive effects existed from the GL phenotype to the liabilities (latent variables) to CD and SB and from the liability to CD to that of SB considering four periods regarding GL. The data contained GL, CD, and SB records from 90,393 primiparous cows, sired by 1122 bulls, distributed over 935 herd-calving year classes. Low genetic correlations between GL and the other calving traits were found, whereas the liabilities to CD and SB were high and positively correlated, genetically. The model indicated that gestations of ∼274 days of length (3 days shorter than the average) would lead to the lowest CD and SB and confirmed the existence of an intermediate optimum of GL with respect to these traits.
Long-Term Effects of Inducible Mutagenic DNA Repair on Relative Fitness and Phenotypic Diversification in Pseudomonas cichorii 302959
Authors: Weigand Michael R , Sundin George W 
Published: November 2008

Abstract
Mutagenic DNA repair (MDR) employs low-fidelity DNA polymerases capable of replicating past DNA lesions resulting from exposure to high-energy ultraviolet radiation (UVR). MDR confers UVR tolerance and activation initiates a transient mutator phenotype that may provide opportunities for adaptation. To investigate the potential role of MDR in adaptation, we have propagated parallel lineages of the highly mutable epiphytic plant pathogen Pseudomonas cichorii 302959 with daily UVR activation (UVR lineages) for ∼500 generations. Here we examine those lineages through the measurement of relative fitness and observation of distinct colony morphotypes that emerged. Isolates and population samples from UVR lineages displayed gains in fitness relative to the ancestor despite increased rates of inducible mutation to rifampicin resistance. Regular activation of MDR resulted in the maintenance of genetic diversity within UVR lineages, including the reproducible diversification and coexistence of “round” and “fuzzy” colony morphotypes. These results suggest that inducible mutability may present a reasonable strategy for adaptive evolution in stressful environments by contributing to gains in relative fitness and diversification.
Simple Telomeres in a Simple Animal: Absence of Subtelomeric Repeat Regions in the PlacozoanTrichoplax adhaerens
Authors: Robertson Hugh M 
Published: November 2008

AbstractSimple telomeres were identified in the genome assembly of the basal placozoan animal Trichoplax adhaerens. They have 1–2 kb of TTAGGG telomeric repeats, which are preceded by a subtelomeric region of 1.5–13 kb. Unlike subtelomeric regions in most animals examined, these subtelomeric regions are unique to each telomere.
Association Between Parapneumonic Effusion and Pericardial Effusion in a Pediatric Cohort
Authors: Roberts Jon E. , Bezack Brian J. , Winger David I. , Pollack Simcha , Shah Rakesh A. , Cataletto Mary , Katz Douglas S. , Montoya-Iraheta Carlos , Schroeder Scott A. , Quintos-Alagheband Maria Lyn 
Published: November 2008

OBJECTIVE. Associations between pleural and pericardial effusions have been described in malignancy and autoimmune disorders. Bacterial pneumonia is the most frequent cause of parapneumonic effusion; however, knowledge of the relationship between parapneumonic effusion and the presence of pericardial fluid in children is limited. We examined this relationship.
METHODS. We performed a retrospective chart review of pediatric patients who were admitted to our institution during a 6-year period with a diagnosis of either parapneumonic effusion or empyema and who had undergone an echocardiogram, a computed tomography scan of the thorax, or both. All demographic, clinical, radiographic, and laboratory data of these patients were collected, and statistical analysis was done with Student's t tests and χ2 analyses.
RESULTS. We reviewed the charts of 59 children with parapneumonic effusions. Forty-eight underwent 2-dimensional echocardiography, chest computed tomography scan, or both. Of these 48 patients, 54.2% (n = 26) were found to have a concomitant pericardial effusion. The majority of patients with pericardial effusions had left-sided pleural disease. Patients with pericardial effusions had more symptomatic days before hospitalization, lower pleural fluid albumin levels, elevated serum white blood cell counts, elevated pleural fluid white blood cell and absolute neutrophil counts, and an increased incidence of surgical intervention. One patient had evidence of hemodynamic compromise that required pericardiocentesis.
CONCLUSIONS. We found a high incidence of pericardial effusions in pediatric patients with parapneumonic effusions. Leukocytosis, higher pleural fluid leukocyte and neutrophil counts, and a propensity for surgical intervention suggest a prognostic relationship between pericardial effusions and more severe parapneumonic disease. The majority of these pericardial collections resolve with treatment of the underlying pleural disease.
False-Positive Serum Human Chorionic Gonadotropin (hCG) in a Male Patient with a Malignant Germ Cell Tumor of the Testis: A Case Report and Review of the Literature
Authors: Ballieux Bart E.P.B. , Weijl Nir I. , Gelderblom Hans , van Pelt Johannes , Osanto Susanne 
Published: November 2008

Abstract
A 39-year-old male patient with a favorable prognosis stage IIB metastatic malignant germ cell tumor (GCT) and elevated pre- and postorchiectomy serum human chorionic gonadotropin (hCG) was treated with three courses of combination chemotherapy resulting in a rapid normalization of his serum hCG.
Within 2 months after the cessation of chemotherapy, his serum hCG increased again, suggesting tumor recurrence. Pathological examination of the resected residual retroperitoneal lymph nodes revealed no vital tumor cells. Based on the further rise in his serum hCG and enlargement of mediastinal lymph nodes on computed tomography scan, the patient underwent second- and third-line chemotherapy, which did not result in normalization of his serum hCG. Reanalysis of stored serum samples with other immunoassays revealed that the elevated serum hCG levels collected before first-line chemotherapy were indeed elevated, but those collected after first-line chemotherapy were all falsely positive. Currently, the patient is still alive and disease free.
This is the first report of a male cancer patient who received unneeded second- and third-line chemotherapy for relapse based on false-positive hCG results. We discuss the pitfalls of false-positive serum hCG measurements, including heterophilic antibodies, as in our IgA-deficient patient, and review the literature.
The Clinical Significance of Statistical Significance
Authors: Kane Robert C. 
Published: November 2008

AbstractLearning ObjectivesAfter completing this course, the reader should be able to: Explain the difference between exploratory (hypothesis-generating) analyses and confirmatory (hypothesis-testing) analyses.Describe why a statistical test result (p-value) only expresses the likelihood that the result could have occurred by chance and does not prove the truth of the study.Define what a hazard ratio expresses.CME This article is available for continuing medical education credit at CME.TheOncologist.comModern clinical trials provide the evidence for most therapeutic advances, and that evidence, expressed in a statistical format, is used to draw inferences about a population from the study's results. Clinician judgment translates these inferences for best individual patient care, but many clinicians struggle with the statistical interpretation of trial results. This review provides a clinical and non-Bayesian perspective on some key elements in the statistical design, analysis, and interpretation of randomized, comparative, phase III clinical trials intended to demonstrate a better outcome (superiority) than with a control treatment.
Designing tradeable rights to manage aquifer recharge according to robust separation principles
Authors: Ward John , Dillon Peter , Grandgirard Agnes 
Published: November 2008

Many cities are experiencing mature urban water economies, characterised by limited opportunities for future water impoundments, rising incremental supply and infrastructure costs, intensified competition and increased interdependencies between diverse water uses. Aquifer storage and recovery (ASR) is currently promoted as one option to augment existing supplies and in many jurisdictions is assuming increasing importance in the portfolio of urban water management strategies. Consistent with trends in international water policy development, Australian water reform has emphasised institutional and governance approaches promoting voluntary transfers of water through market exchange. The reform process has made substantial advances in addressing the constraints and tensions associated with mature rural water economies, with limited influence in urban water systems.
What remains unclear is the degree of alignment of new water management technologies such as ASR operations with explicit water reform directives of market development and the capacity of subsequent urban water legislation to provide consistent and coherent ASR guidelines.
The paper describes a systematic approach to align the hydrological characteristics of an aquifer with economic and policy interpretations central to the development and management of ASR. The paper introduces a schema to identify the elements of the urban terrestrial water cycle specific to ASR, the development of a typology to characterise the aquifer potential for ASR, and identify and determine the nature of property rights for each system element according to the principles of robust separation of water rights.
Xenin, a Gastrointestinal Peptide, Regulates Feeding Independent of the Melanocortin Signaling Pathway
Authors: Leckstrom Arnold , Kim Eun Ran , Wong Davie , Mizuno Tooru M. 
Published: November 2008

OBJECTIVE—Xenin, a 25–amino acid peptide, was initially isolated from human gastric mucosa. Plasma levels of xenin rise after a meal in humans, and administration of xenin inhibits feeding in rats and chicks. However, little is known about the mechanism by which xenin regulates food intake. Signaling pathways including leptin and melanocortins play a pivotal role in the regulation of energy balance. Therefore, we addressed the hypothesis that xenin functions as a satiety factor by acting through the melanocortin system or by interacting with leptin.
RESEARCH DESIGN AND METHODS—The effect of intracerebroventricular and intraperitoneal administration of xenin on food intake was examined in wild-type, agouti, and ob/ob mice. The effect of intracerebroventricular injection of SHU9119, a melanocortin receptor antagonist, on xenin-induced anorexia was also examined in wild-type mice. To determine whether the hypothalamus mediates the anorectic effect of xenin, we examined the effect of intraperitoneal xenin on hypothalamic Fos expression.
RESULTS—Both intracerebroventricular and intraperitoneal administration of xenin inhibited fasting-induced hyperphagia in wild-type mice in a dose-dependent manner. The intraperitoneal injection of xenin also reduced nocturnal intake in ad libitum–fed wild-type mice. The intraperitoneal injection of xenin increased Fos immunoreactivity in hypothalamic nuclei, including the paraventricular nucleus and the arcuate nucleus. Xenin reduced food intake in agouti and ob/ob mice. SHU9119 did not block xenin-induced anorexia.
CONCLUSIONS—Our data suggest that xenin reduces food intake partly by acting through the hypothalamus but via signaling pathways that are independent of those used by leptin or melanocortins.
IddLoci Synergize to Prolong Islet Allograft Survival Induced by Costimulation Blockade in NOD Mice
Authors: Mangada Julie , Pearson Todd , Brehm Michael A. , Wicker Linda S. , Peterson Laurence B. , Shultz Leonard D. , Serreze David V. , Rossini Aldo A. , Greiner Dale L. 
Published: November 2008

OBJECTIVE—NOD mice model human type 1 diabetes and are used to investigate tolerance induction protocols for islet transplantation in a setting of autoimmunity. However, costimulation blockade–based tolerance protocols have failed in prolonging islet allograft survival in NOD mice.RESEARCH DESIGN AND METHODS—To investigate the underlying mechanisms, we studied the ability of costimulation blockade to prolong islet allograft survival in congenic NOD mice bearing insulin-dependent diabetes (Idd) loci that reduce the frequency of diabetes.RESULTS—The frequency of diabetes is reduced in NOD.B6 Idd3 mice and is virtually absent in NOD.B6/B10 Idd3 Idd5 mice. Islet allograft survival in NOD.B6 Idd3 mice treated with costimulation blockade is prolonged compared with NOD mice, and in NOD.B6/B10 Idd3 Idd5, mice islet allograft survival is similar to that achieved in C57BL/6 mice. Conversely, some Idd loci were not beneficial for the induction of transplantation tolerance. Alloreactive CD8 T-cell depletion in (NOD × CBA)F1 mice treated with costimulation blockade was impaired compared with similarly treated (C57BL/6.H2g7 × CBA)F1 mice. Injection of exogenous interleukin (IL)-2 into NOD mice treated with costimulation prolonged islet allograft survival. NOD.B6 Idd3 mice treated with costimulation blockade deleted alloreactive CD8 T-cells and exhibited prolonged islet allograft survival.CONCLUSIONS— Il2 is the Idd3 diabetes susceptibility gene and can influence the outcome of T-cell deletion and islet allograft survival in mice treated with costimulation blockade. These data suggest that Idd loci can facilitate induction of transplantation tolerance by costimulation blockade and that IL-2/Idd3 is a critical component in this process.
Hypoxia Decreases Insulin Signaling Pathways in Adipocytes
Authors: Regazzetti Claire , Peraldi Pascal , Grémeaux Thierry , Najem-Lendom Rosanna , Ben-Sahra Issam , Cormont Mireille , Bost Frédéric , Le Marchand-Brustel Yannick , Tanti Jean-François , Giorgetti-Peraldi Sophie 
Published: November 2008

OBJECTIVE—Obesity is characterized by an overgrowth of adipose tissue that leads to the formation of hypoxic areas within this tissue. We investigated whether this phenomenon could be responsible for insulin resistance by studying the effect of hypoxia on the insulin signaling pathway in adipocytes.
RESEARCH DESIGN AND METHODS—The hypoxic signaling pathway was modulated in adipocytes from human and murine origins through incubation under hypoxic conditions (1% O2) or modulation of hypoxia-inducible factor (HIF) expression. Insulin signaling was monitored through the phosphorylation state of several key partners of the pathway and glucose transport.
RESULTS—In both human and murine adipocytes, hypoxia inhibits insulin signaling as revealed by a decrease in the phosphorylation of insulin receptor. In 3T3-L1 adipocytes, this inhibition of insulin receptor phosphorylation is followed by a decrease in the phosphorylation state of protein kinase B and AS160, as well as an inhibition of glucose transport in response to insulin. These processes were reversible under normoxic conditions. The mechanism of inhibition seems independent of protein tyrosine phosphatase activities. Overexpression of HIF-1α or -2α or activation of HIF transcription factor with CoCl2 mimicked the effect of hypoxia on insulin signaling, whereas downregulation of HIF-1α and -2α by small interfering RNA inhibited it.
CONCLUSIONS—We have demonstrated that hypoxia creates a state of insulin resistance in adipocytes that is dependent upon HIF transcription factor expression. Hypoxia could be envisioned as a new mechanism that participates in insulin resistance in adipose tissue of obese patients.
Site-Specific GlcNAcylation of Human Erythrocyte Proteins
Authors: Wang Zihao , Park Kyoungsook , Comer Frank , Hsieh-Wilson Linda C. , Saudek Christopher D. , Hart Gerald W. 
Published: November 2008

OBJECTIVE— O-linked N-acetylglucosamine (O-GlcNAc) is upregulated in diabetic tissues and plays a role in insulin resistance and glucose toxicity. Here, we investigated the extent of GlcNAcylation on human erythrocyte proteins and compared site-specific GlcNAcylation on erythrocyte proteins from diabetic and normal individuals.
RESEARCH DESIGN AND METHODS—GlcNAcylated erythrocyte proteins or GlcNAcylated peptides were tagged and selectively enriched by a chemoenzymatic approach and identified by mass spectrometry. The enrichment approach was combined with solid-phase chemical derivatization and isotopic labeling to detect O-GlcNAc modification sites and to compare site-specific O-GlcNAc occupancy levels between normal and diabetic erythrocyte proteins.
RESULTS—The enzymes that catalyze the cycling (addition and removal) of O-GlcNAc were detected in human erythrocytes. Twenty-five GlcNAcylated erythrocyte proteins were identified. Protein expression levels were compared between diabetic and normal erythrocytes. Thirty-five O-GlcNAc sites were reproducibly identified, and their site-specific O-GlcNAc occupancy ratios were calculated.
CONCLUSIONS—GlcNAcylation is differentially regulated at individual sites on erythrocyte proteins in response to glycemic status. These data suggest not only that site-specific O-GlcNAc levels reflect the glycemic status of an individual but also that O-GlcNAc site occupancy on erythrocyte proteins may be eventually useful as a diagnostic tool for the early detection of diabetes.
Methyltransferase Set7/9 Maintains Transcription and Euchromatin Structure at Islet-Enriched Genes
Authors: Deering Tye G. , Ogihara Takeshi , Trace Anthony P. , Maier Bernhard , Mirmira Raghavendra G. 
Published: November 2008

OBJECTIVE—The activation of β-cell genes, particularly of those encoding preproinsulin, requires an appropriate euchromatin (or “open”) DNA template characterized by hypermethylation of Lys4 of histone H3. We hypothesized that this modification is maintained in islet β-cells by the action of the histone methyltransferase Set7/9.
RESEARCH DESIGN AND METHODS—To identify the role of Set7/9, we characterized its expression pattern and gene regulation and studied its function using RNA interference in both cell lines and primary mouse islets.
RESULTS—Within the pancreas, Set7/9 protein shows striking specificity for islet cells, including α- and β-cells, as well as occasional cells within ducts. Consistent with these findings, the Set7/9 gene promoter contained an islet-specific enhancer located between −5,768 and −6,030 base pairs (relative to the transcriptional start site) that exhibited Pdx1-responsive activation in β-cells. To study Set7/9 function, we depleted insulinoma cells and primary mouse islets of Set7/9 protein using siRNA. Following siRNA treatment, we observed striking repression of genes involved in glucose-stimulated insulin secretion, including Ins1/2, Glut2, and MafA. These changes in transcription were accompanied by loss of dimethylated H3 Lys4 and RNA polymerase II recruitment, particularly at the Ins1/2 and Glut2 genes. Consistent with these data, depletion of Set7/9 in islets led to defects in glucose-stimulated Ca2+ mobilization and insulin secretion.
CONCLUSIONS—We conclude that Set7/9 is required for normal β-cell function, likely through the maintenance of euchromatin structure at genes necessary for glucose-stimulated insulin secretion.
Trends in Postpartum Diabetes Screening and Subsequent Diabetes and Impaired Fasting Glucose Among Women With Histories of Gestational Diabetes Mellitus
Authors: Ferrara Assiamira , Peng Tiffany , Kim Catherine 
Published: November 2008

OBJECTIVE—The purpose of this study was to examine trends in postpartum glucose screening for women with gestational diabetes mellitus (GDM), predictors of screening, trends in postpartum impaired fasting glucose (IFG) and diabetes, and diabetes and pre-diabetes detected by postpartum fasting plasma glucose (FPG) versus a 75-g oral glucose tolerance test (OGTT).
RESEARCH DESIGN AND METHODS—This was a cohort study of 14,448 GDM pregnancies delivered between 1995 and 2006. Postpartum screening was defined as performance of either an FPG or OGTT at least 6 weeks after delivery and within 1 year of delivery.
RESULTS—Between 1995 and 2006, the age- and race/ethnicity-adjusted proportion of women who were screened postpartum rose from 20.7% (95% CI 17.8–23.5) to 53.8% (51.3–56.3). Older age, Asian or Hispanic race/ethnicity, higher education, earlier GDM diagnosis, use of diabetes medications during pregnancy, and more provider contacts after delivery were independent predictors of postpartum screening. Obesity and higher parity were independently associated with lower screening performance. Among women who had postpartum screening, the age- and race/ethnicity-adjusted proportion of IFG did not change over time (24.2 [95% CI 20.0–27.8] in 1995–1997 to 24.3 [22.6–26.0] in 2004–2006), but the proportion of women with diabetes decreased from 6.1 (95% CI 4.2–8.1) in 1995–1997 to 3.3 (2.6–4.0) in 2004–2006. Among women who received an OGTT in 2006, 38% of the 204 women with either diabetes or pre-diabetes were identified only by the 2-h glucose measurements.
CONCLUSIONS—Postpartum screening has increased over the last decade, but it is still suboptimal. Compared with FPGs alone, the 2-h values identify a higher proportion of women with diabetes or pre-diabetes amenable to intervention.
Pitfalls in the Measurement of the Nocturnal Blood Pressure Dip in Adolescents with Type 1 Diabetes
Authors: Delaney Angela , Pellizzari Margaret , Speiser Phyllis W. , Frank Graeme R. 
Published: November 2008

OBJECTIVE—The purpose of this study was to screen adolescents with type 1 diabetes using ambulatory blood pressure monitoring (ABPM) to 1) test the hypothesis that using a preset sleep time results in an overdiagnosis of abnormal nocturnal dipping in systolic blood pressure and 2) assess the reproducibility of an abnormal nocturnal systolic blood pressure dip.
RESEARCH DESIGN AND METHODS—For aim 1, ABPM from 53 adolescent patients with type 1 diabetes was reviewed. Nocturnal dips in systolic blood pressure calculated by actual sleep time were compared with those from a preset sleep time. For aim 2, blood pressure monitoring from 98 patients using actual reported sleep time was reviewed. Reproducibility of the nocturnal dip in systolic blood pressure was assessed in a subset of “nondippers.”
RESULTS—For aim 1, the actual mean ± SE decline in nocturnal systolic blood pressure was 11.6 ± 4.7%, whereas the mean decline in nocturnal systolic blood pressure calculated using the preset sleep time was 8.8 ± 4.9% (P &lt; 0.0001). For aim 2, 64% of patients had a normal nocturnal decline in systolic blood pressure (14.9 ± 3.1% mmHg), whereas 36% had an abnormal dip (5.7 ± 2.8% mmHg). Repeat ABPM performed in 22 of the 35 nondippers revealed that only 36% had abnormal systolic dipping confirmed on the repeat ABPM.
CONCLUSIONS—The use of actual reported sleep time is required to accurately determine the nocturnal dip in systolic blood pressure. Repeating ABPM in nondippers is essential to confirm this abnormality.