bluuebunny/crossref_metadata_2025_split huggingface dataset:
Results of Data Verification of the Japan Congenital Cardiovascular Database, 2008 to 2009
Authors: Tomotaki Ai , Miyata Hiroaki , Hashimoto Hideki , Murakami Arata , Ono Minoru 
Published: January 2014

Background: Since 2008, data concerning pediatric cardiovascular surgeries performed in Japan have been collected in the Japan Congenital Cardiovascular Surgery Database (JCCVSD). We assessed the quality of the JCCVSD data through data verification activities conducted in 2010. Methods: During 2008 to 2009, 3345 patients with 4327 procedures at 25 hospitals were registered in the JCCVSD. Among them, six sites were selected for data verification. The completeness of case registration was assessed by comparison with original operational logs. Also, data accuracy of patient demographics, surgical outcomes, and processes were assessed with 10% of the registered cases by comparison with medical records. Results: Verification of case registration completeness involved 968 (28.9%) patients and 1279 (29.1%) procedures. As to completeness, we confirmed 1266 (99.0%) of the 1279 procedures. Data accuracy was verified for 129 (3.9%) patients. Accuracy of status of discharge and 30 and 90 days after surgery were very high (99.2%, 100%, and 100%, respectively). Data items with numeric information exhibited lower exact accuracy due to typing error and inconsistent use of rounding; however, the differences between the submitted and the original data were not statistically significant. Conclusions: High completeness and acceptable range of data accuracy were verified for the data submitted to the JCCVSD in 2008 to 2009. The high accuracy regarding follow-up outcomes was especially noteworthy. The initial success of the JCCVSD should be strengthened through further sophistication of registration protocol, continual training of data managers and auditors, and rigorous expansion of verification activities.
Determining cell-of-origin subtypes of diffuse large B-cell lymphoma using gene expression in formalin-fixed paraffin-embedded tissue
Authors: Scott David W. , Wright George W. , Williams P. Mickey , Lih Chih-Jian , Walsh William , Jaffe Elaine S. , Rosenwald Andreas , Campo Elias , Chan Wing C. , Connors Joseph M. , Smeland Erlend B. , Mottok Anja , Braziel Rita M. , Ott German , Delabie Jan , Tubbs Raymond R. , Cook James R. , Weisenburger Dennis D. , Greiner Timothy C. , Glinsmann-Gibson Betty J. , Fu Kai , Staudt Louis M. , Gascoyne Randy D. , Rimsza Lisa M. 
Published: January 2014

Key Points
A 20-gene gene expression-based assay accurately and robustly assigns COO subtypes of DLBCL using formalin-fixed paraffin-embedded tissue.
Dental caries and erosion status of 12-year-old Hong Kong children
Authors: Zhang Shinan , Chau Alex MH , Lo Edward CM , Chu Chun-Hung 
Published: January 2014

Abstract

Background
This study aimed to assess the dental caries and erosion status of 12-year-old Hong Kong children and study the determinants of dental caries and dental erosion of these children.

Methods
The survey was performed from 2011 to 2012 with ethics approval. Stratified random sampling was adopted to select 12-year-old children in 7 primary schools in Hong Kong. The participating parents were asked to complete a self-administered questionnaire concerning their children’s diet and oral health habits. The children were examined for caries status with WHO criteria by 3 calibrated examiners. Detection of dental erosion followed Basic Erosive Wear Examination (BEWE) criteria.

Results
A total of 704 children were recruited and 600 (316 boys, 53%) participated in the survey. There were 124 children (21%) with caries experience (DMFT > 0) and their DMFT was 0.34 ± 0.76. About half of their decay was unfilled (DT = 0.16 ± 0.52) The DMFT of girls and boys were 0.45 ± 0.89 and 0.23 ± 0.61, respectively (p = 0.001). Girls also had a higher DT (0.21 ± 0.62 compared with 0.11 ± 0.41, p = 0.013) and FT than boys (0.23 ± 0.63 compared with 0.12 ± 0.44, p = 0.016). Most children (75%) had at least some sign of erosion (BEWE > 0), but no severe erosion (BEWE = 3). Logistic regression showed girls who consumed soft drinks and took vitamin C supplements had higher caries risk. Dental erosion was more severe among the children who had caries experience and consumed fruit juice.

Conclusions
The 12-year-old Hong Kong children had low caries experience, and almost half of the decay was left untreated. Although severe erosion was not found, many children had early signs of erosion.
Enhanced resistive switching phenomena using low-positive-voltage format and self-compliance IrO
x
/GdO
x
/W cross-point memories
Authors: Jana Debanjan , Maikap Siddheswar , Prakash Amit , Chen Yi-Yan , Chiu Hsien-Chin , Yang Jer-Ren 
Published: January 2014

Abstract
Enhanced resistive switching phenomena of IrO
x
/GdO
x
/W cross-point memory devices have been observed as compared to the via-hole devices. The as-deposited Gd2O3 films with a thickness of approximately 15 nm show polycrystalline that is observed using high-resolution transmission electron microscope. Via-hole memory device shows bipolar resistive switching phenomena with a large formation voltage of -6.4 V and high operation current of >1 mA, while the cross-point memory device shows also bipolar resistive switching with low-voltage format of +2 V and self-compliance operation current of <300 μA. Switching mechanism is based on the formation and rupture of conducting filament at the IrO
x
/GdO
x
interface, owing to oxygen ion migration. The oxygen-rich GdO
x
layer formation at the IrO
x
/GdO
x
interface will also help control the resistive switching characteristics. This cross-point memory device has also Repeatable 100 DC switching cycles, narrow distribution of LRS/HRS, excellent pulse endurance of >10,000 in every cycle, and good data retention of >104 s. This memory device has great potential for future nanoscale high-density non-volatile memory applications.
Neuroendocrinology of the Skin1
Authors: Slominski Andrzej , Wortsman Jacobo 
Published: January 2014

AbstractThe classical observations of the skin as a target for melanotropins have been complemented by the discovery of their actual production at the local level. In fact, all of the elements controlling the activity of the hypothalamus-pituitary-adrenal axis are expressed in the skin including CRH, urocortin, and POMC, with its products ACTH, α-MSH, and β-endorphin. Demonstration of the corresponding receptors in the same cells suggests para- or autocrine mechanisms of action. These findings, together with the demonstration of cutaneous production of numerous other hormones including vitamin D3, PTH-related protein (PTHrP), catecholamines, and acetylcholine that share regulation by environmental stressors such as UV light, underlie a role for these agents in the skin response to stress. The endocrine mediators with their receptors are organized into dermal and epidermal units that allow precise control of their activity in a field-restricted manner. The skin neuroendocrine system communicates with itself and with the systemic level through humoral and neural pathways to induce vascular, immune, or pigmentary changes, to directly buffer noxious agents or neutralize the elicited local reactions. Therefore, we suggest that the skin neuroendocrine system acts by preserving and maintaining the skin structural and functional integrity and, by inference, systemic homeostasis.
Pathophysiology and Pharmacological Treatment of Insulin Resistance*
Authors: Matthaei Stephan , Stumvoll Michael , Kellerer Monika , Häring Hans-Ulrich 
Published: January 2014

AbstractDiabetes mellitus type 2 is a world-wide growing health problem affecting more than 150 million people at the beginning of the new millennium. It is believed that this number will double in the next 25 yr. The pathophysiological hallmarks of type 2 diabetes mellitus consist of insulin resistance, pancreatic β-cell dysfunction, and increased endogenous glucose production. To reduce the marked increase of cardiovascular mortality of type 2 diabetic subjects, optimal treatment aims at normalization of body weight, glycemia, blood pressure, and lipidemia. This review focuses on the pathophysiology and molecular pathogenesis of insulin resistance and on the capability of antihyperglycemic pharmacological agents to treat insulin resistance, i.e., α-glucosidase inhibitors, biguanides, thiazolidinediones, sulfonylureas, and insulin. Finally, a rational treatment approach is proposed based on the dynamic pathophysiological abnormalities of this highly heterogeneous and progressive disease.
Autoimmune Adrenal Insufficiency and Autoimmune Polyendocrine Syndromes: Autoantibodies, Autoantigens, and Their Applicability in Diagnosis and Disease Prediction
Authors: Betterle Corrado , Dal Pra Chiara , Mantero Franco , Zanchetta Renato 
Published: January 2014

AbstractRecent progress in the understanding of autoimmune adrenal disease, including a detailed analysis of a group of patients with Addison’s disease (AD), has been reviewed. Criteria for defining an autoimmune disease and the main features of autoimmune AD (history, prevalence, etiology, histopathology, clinical and laboratory findings, cell-mediated andhumoral immunity, autoantigens and their autoepitopes, genetics, animal models, associated autoimmune diseases, pathogenesis, natural history, therapy) have been described. Furthermore, the autoimmune polyglandular syndromes (APS) associated with AD (revised classification, animal models, genetics, natural history) have been discussed.Of Italian patients with primary AD (n = 317), 83% had autoimmune AD. At the onset, all patients with autoimmune AD (100%) had detectable adrenal cortex and/or steroid 21-hydroxylase autoantibodies. In the course of natural history of autoimmune AD, the presence of adrenal cortex and/or steroid 21-hydroxylase autoantibodies identified patients at risk to develop AD. Different risks of progression to clinical AD were found in children and adults, and three stages of subclinical hypoadrenalism have been defined. Normal or atrophic adrenal glands have been demonstrated by imaging in patients with clinical or subclinical AD.Autoimmune AD presented in four forms: as APS type 1 (13% of the patients), APS type 2 (41%), APS type 4 (5%), and isolated AD (41%). There were differences in genetics, age at onset, prevalence of adrenal cortex/21-hydroxylase autoantibodies, and associated autoimmune diseases in these groups. “Incomplete” forms of APS have been identified demonstrating that APS are more prevalent than previously reported.A varied prevalence of hypergonadotropic hypogonadism in patients with AD and value of steroid-producing cells autoantibodies reactive with steroid 17α-hydroxylase or P450 side-chain cleavage enzyme as markers of this disease has been discussed. In addition, the prevalence, characteristic autoantigens, and autoantibodies of minor autoimmune diseases associated with AD have been described.Imaging of adrenal glands, genetic tests, and biochemical analysis have been shown to contribute to early and correct diagnosis of primary non-autoimmune AD in the cases of hypoadrenalism with undetectable adrenal autoantibodies. An original flow chart for the diagnosis of AD has been proposed.
Are There Any Sensitive and Specific Sex Steroid Markers for Polycystic Ovary Syndrome?
Authors: Stener-Victorin Elisabet , Holm Göran , Labrie Fernand , Nilsson Lars , Janson Per Olof , Ohlsson Claes 
Published: January 2014

ABSTRACT

Context
Despite the high prevalence of hyperandrogenemia, the principal biochemical abnormality in women with polycystic ovary syndrome (PCOS), a definitive endocrine marker for PCOS has so far not been identified.

Objective
To identify a tentative diagnostic marker for PCOS, we compared serum levels of sex steroids, their precursors, and main metabolites in women with PCOS and controls.

Design and Methods
In this cross-sectional study of 74 women with PCOS and 31 controls, we used gas and liquid chromatography/mass spectrometry to analyze serum sex steroid precursors, estrogens, androgens, and glucuronidated androgen metabolites; performed immunoassays of SHBG, LH, and FSH; and calculated the LH/FSH ratio.

Results
Androgens and estrogens, sex steroid precursors, and glucuronidated androgen metabolites were higher in women with PCOS than in controls. In multivariate logistic regression analyses, estrone and free testosterone were independently associated with PCOS. The odds ratios per sd increase were 24.2 for estrone [95% confidence interval (CI), 4.0-144.7] and 12.8 for free testosterone (95% CI, 3.1-53.4). In receiver operating characteristic analyses, the area under curve was 0.93 for estrone (95% CI, 0.88-0.98) and 0.91 for free testosterone (95% CI, 0.86-0.97), indicating high sensitivity and specificity.

Conclusion
Women with PCOS have elevated levels of sex steroid precursors, estrogens, androgens, and glucuronidated androgen metabolites as measured with a specific and sensitive mass spectrometry-based technique. The combination of elevated estrone (&gt;50 pg/ml) and free testosterone (&gt;3.3 pg/ml) appeared to discriminate with high sensitivity and specificity between women with and without PCOS.
Glucagon Deficiency Reduces Hepatic Glucose Production and Improves Glucose Tolerance In Adult Mice
Authors: Hancock Aidan S. , Du Aiping , Liu Jingxuan , Miller Mayumi , May Catherine L. 
Published: January 2014

Abstract
The major role of glucagon is to promote hepatic gluconeogenesis and glycogenolysis to raise blood glucose levels during hypoglycemic conditions. Several animal models have been established to examine the in vivo function of glucagon in the liver through attenuation of glucagon via glucagon receptor knockout animals and pharmacological interventions. To investigate the consequences of glucagon loss to hepatic glucose production and glucose homeostasis, we derived mice with a pancreas specific ablation of the α-cell transcription factor, Arx, resulting in a complete loss of the glucagon-producing pancreatic α-cell. Using this model, we found that glucagon is not required for the general health of mice but is essential for total hepatic glucose production. Our data clarifies the importance of glucagon during the regulation of fasting and postprandial glucose homeostasis.
Adrenomedullin Relaxes Rat Uterine Artery: Mechanisms and Influence of Pregnancy and Estradiol
Authors: Ross Gracious R. , Yallampalli Uma , Gangula Pandu R. R. , Reed Luckey , Sathishkumar K. , Gao Haijun , Chauhan Madhu , Yallampalli Chandra 
Published: January 2014

Abstract
Uterine arteries play a major role in regulating uteroplacental blood flow. Failure to maintain blood flow to the uteroplacental compartment during pregnancy often results in intrauterine growth retardation. Immunohistochemical staining of adrenomedullin (AM), an endogenous vasoactive peptide, in uterine artery was intense in pregnant compared to nonpregnant rats, but it is not known whether AM directly relaxes uterine artery or not. In this study, we elucidated the mechanisms of uterine artery relaxation by AM and its regulation by pregnancy and female sex steroids. AM was able to relax uterine artery, and this relaxation was influenced positively by pregnancy and estradiol as evidenced by the increased pD2 and Emax values of AM. Both pregnancy and estradiol treatment to ovariectomized rats amplified RAMP3 expression in uterine arteries while progesterone had no effect. AM-induced uterine artery relaxation is predominantly endothelium-dependent. The AM receptor antagonist CGRP8-37 is more potent than AM22-52 in inhibiting the AM relaxation, indicating the involvement of AM2 receptor subtype. Moreover, AM uses the classical nitric oxide-cGMP pathway along with KCa channels to mediate the vasodilatory effect in uterine artery. In conclusion, sensitivity of uterine artery to AM-induced relaxation is increased with pregnancy or estradiol treatment by increasing RAMP3 expression, suggesting an important role for AM in regulating the uterine hemodynamics, probably maintaining uterine blood flow during pregnancy and in pre- and postmenopausal cardiovascular adaptation differences.
Large Litter Rearing Enhances Leptin Sensitivity and Protects Selectively Bred Diet-induced Obese Rats from Becoming Obese
Authors: Patterson Christa M. , Bouret Sebastien G. , Park Sunny , Irani Boman G. , Dunn-Meynell Ambrose A. , Levin Barry E. 
Published: January 2014

Abstract
Because rearing rats in large litters (LLs) protects them from becoming obese, we postulated that LL rearing would protect rats selectively bred to develop diet-induced obesity (DIO) from becoming obese by overcoming their inborn central leptin resistance. Male and female DIO rats were raised in normal litters (10 pups/dam) or LLs (16 pups/dam) and assessed for anatomical, biochemical, and functional aspects of leptin sensitivity at various ages when fed low-fat chow or a 31% fat high-energy (HE) diet. LL rearing reduced plasma leptin levels by postnatal d 2 (P) 2 and body weight gain by P8. At P16, LL DIO neonates had increased arcuate nucleus (ARC) binding of leptin to its extracellular receptors and at P28 an associated increase of their agouti-related peptide and α-MSH axonal projections to the paraventricular nucleus. Reduced body weight persisted and was associated with increased ARC leptin receptor binding and sensitivity to the anorectic effects of leptin, reduced adiposity, and enhanced insulin sensitivity in LL DIO rats fed chow until 10 wk of age. The enhanced ARC leptin receptor binding and reduced adiposity of LL DIO rats persisted after an additional 5 wk on the HE diet. Female LL DIO rats had similar reductions in weight gain on both chow and HE diet vs. normal litter DIO rats. We postulate that LL rearing enhances DIO leptin sensitivity by lowering plasma leptin levels and thereby increasing leptin receptor availability and that this both enhances the ARC-paraventricular nucleus pathway development and protects them from becoming obese.
Comparable Sensitivity of Postmenopausal and Young Women to the Effects of Intranasal Insulin on Food Intake and Working Memory
Authors: Krug Rosemarie , Benedict Christian , Born Jan , Hallschmid Manfred 
Published: January 2014

ABSTRACT

Context
We have previously shown that enhancing brain insulin signaling by intranasal administration of a single dose of the hormone acutely reduces food intake in young men but not women, whereas its improving effects on spatial and working memory are restricted to young women.

Objective
Against the background of animal studies suggesting that low estrogen concentrations are a prerequisite for the anorexigenic impact of central nervous insulin, we extended our foregoing study by assessing intranasal insulin effects in postmenopausal women with comparatively low estrogen concentrations, expecting them to be more sensitive than young women to the anorexigenic effects of the hormone.

Design, Setting, Participants, and Intervention
In a within-subject, double-blind comparison performed at the University of Lübeck, 14 healthy postmenopausal women (body mass index, 23.71 ± 0.6 kg/m2; age, 57.61 ± 1.14 yr) were intranasally administered 160 IU regular human insulin or vehicle.

Main Outcome Measures
Subjects performed a working memory task (digit span) and a hippocampus-dependent visuospatial memory task. Subsequently, free-choice food intake from an ad libitum breakfast buffet was measured.

Results
Contrary to expectations, results in postmenopausal women mirrored those found in young women (22.44 ± 0.63 yr), i.e. insulin administration did not affect food intake (P &gt; 0.46), but did enhance performance in the prefrontal cortex-dependent working memory task (P &lt; 0.05).

Conclusions
Low estrogen levels as present in postmenopausal women do not modulate the effects of intranasal insulin in females, suggesting that in humans as opposed to rats, estrogen signaling does not critically alter central nervous system sensitivity to the effects of insulin on energy homeostasis and cognition.
Increased Psychopathology and Maladaptive Personality Traits, But Normal Cognitive Functioning, In Patients after Long-Term Cure of Acromegaly
Authors: Tiemensma Jitske , Biermasz Nienke R. , van der Mast Roos C. , Wassenaar Moniek J. E. , Middelkoop Huub A. M. , Pereira Alberto M. , Romijn Johannes A. 
Published: January 2014

ABSTRACT

Objective
Active acromegaly is associated with psychopathology, personality changes, and cognitive dysfunction. It is unknown whether, and to what extent, these effects are present after long-term cure of acromegaly.

Aim
The aim of the study was to assess psychopathology, personality traits, and cognitive function in patients after long-term cure of acromegaly.

Design
This was a cross-sectional study.

Patients and Methods
We studied 68 patients after long-term cure (13 ± 1 yr) of acromegaly and 68 matched controls. We compared these data with 60 patients treated for nonfunctioning pituitary macroadenomas (NFMAs) and 60 matched controls. Psychopathology was assessed using the Apathy Scale, Irritability Scale, Hospital Anxiety and Depression Scale, and Mood and Anxiety Symptoms Questionnaire short-form and personality by the Dimensional Assessment of Personality Pathology short-form (DAPP). Cognitive function was assessed by 11 tests.

Results
Compared with matched controls, patients cured from acromegaly scored significantly worse on virtually all psychopathology questionnaires and on several subscales of the DAPP. Compared with NFMA patients, patients cured from acromegaly scored worse on negative affect (P = 0.050) and somatic arousal (P = 0.009) and seven of 18 subscales of the DAPP (P &lt; 0.05). Cognitive function in patients cured from acromegaly did not differ from matched controls or patients treated for NFMA.

Conclusion
Patients with long-term cure of acromegaly show a higher prevalence of psychopathology and maladaptive personality traits but not cognitive dysfunction, compared with matched controls and patients treated for NFMA. These results suggest irreversible effects of previous GH excess, rather than effects of pituitary adenomas per se and/or their treatment, on the central nervous system.
Molecular Basis for Species and Ligand Specificity of a Monoclonal Antibody Raised Against Human IGF-I
Authors: Van Wyk Judson J. , Bruton Eyvonne T. 
Published: January 2014

Abstract
The anti-hIGF-I monoclonal antibody, α-sm1.2, was found to have substantial crossreactivity with human and rat IGF-II, but recognized rat IGF-I only when this ligand was present at very high concentration. (E50 for hIGF-I ∼3.5 ng/tube vs. ∼12,000 ng/tube for rat IGF-I). In the context of previous studies to define the epitope(s) of α-sm1.2, these findings point to the critical importance of aspartic acid at residue 20 in the B domain in determining the species and ligand specificity of this antibody. Previous studies using this antibody in rodent tissues may require reinterpretation in the light of these findings.