bluuebunny/crossref_metadata_2025_split huggingface dataset:
Catalogs of variable stars, current and future
Authors: Samus Nikolay N. , Kazarovets Elena V. , Durlevich Olga V. 
Published: February 2010

AbstractTo study effects of stellar variability, it is necessary to have complete lists of variable stars with good coordinates, correct variability ranges, reliable classification. The General Catalogue of Variable Stars (GCVS) is one of the main sources of information of this kind. Recently, the flow of information on stellar variability has increased strongly, requiring new approaches to GCVS compilation. New classification schemes are needed for variable stars, taking into account the development of our knowledge. We present information on the current state of the GCVS, its web data base, new Name-Lists containing thousands of new variables. We also discuss the problems of developing a new classification system for variable stars, of implementing catalogs of variable stars based on automatic surveys into the GCVS, of cooperation and interaction between the GCVS and other important sources of information on variable stars.
Biased hosting of intronic microRNA genes
Authors: Golan David , Levy Carmit , Friedman Brad , Shomron Noam 
Published: February 2010

Abstract
Motivation: MicroRNAs (miRNAs) are involved in an abundant class of post-transcriptional regulation activated through binding to the 3′ -untranslated region (UTR) of mRNAs. The current wealth of mammalian miRNA genes results mostly from genomic duplication events. Many of these events are located within introns of transcriptional units. In order to better understand the genomic expansion of miRNA genes, we investigated the distribution of intronic miRNAs.
Results: We observe that miRNA genes are hosted within introns of short genes much larger than expected by chance.
Implementation: We explore several explanations for this phenomenon and conclude that miRNA integration into short genes might be evolutionary favorable due to interaction with the pre-mRNA splicing mechanism.
Contact: nshomron@post.tau.ac.il
Supplementary information: Supplementary data are available at Bioinformatics online.
End‐systolic volume following surgical ventricular reconstruction impacts survival in patients with ischaemic dilated cardiomyopathy
Authors: Di Donato Marisa , Castelvecchio Serenella , Menicanti Lorenzo 
Published: February 2010

AimsA left ventricular end‐systolic volume (LVESV) ≥60 mL/m2 has been shown to be associated with increased cardiac mortality after a reperfused myocardial infarction (MI). The reduction in LVESV following surgical ventricular reconstruction (SVR) is reported to be between 19% and 50% but its impact on prognosis is not well‐established. The aim of this study was therefore to assess the impact on survival of a residual LVESV index (LVESVI) of ≥ or <60 mL/m2 following SVR.Methods and resultsAll patients undergoing SVR at our Centre between July 2001 and March 2009 were eligible to be included in this study if they had a preoperative LVESVI of ≥60 mL/m2 and an LVESVI measurement performed at discharge (7–10 days after surgery). Two hundred and sixteen patients (aged 64 ± 9 years, 33 women) satisfied these criteria. Coronary artery bypass graft was performed in 197 patients (91.2%) and mitral repair in 63 patients (29%). Left ventricular ESVI had decreased by 41% at discharge in the overall population. Patients were grouped according to the residual LVESVI at discharge as follows: Group 1, LVESVI ≥ 60 mL/m2 (n = 71), and Group 2, LVESVI < 60 mL/m2 (n = 145). In both groups, LVESVI decreased significantly with respect to baseline, by 29% in Group 1 and by 47% in Group 2. At multivariate analysis, the presence of a non‐Q‐wave MI and a preoperative internal diastolic diameter of 65 mm were the strongest predictors of a residual post‐operative LVESVI of ≥60 mL/m2. Risk of all‐cause death was significantly higher in Group 1. Post‐operative LVESVI of ≥60 mL/m2 was an independent predictor of mortality at follow‐up [Exp(B) = 10.7, CI: 2.67–42.9, P = 0.001].ConclusionOur findings confirm the role of LVESVI in predicting survival following SVR; the lack of additional improvement in survival with SVR observed in the STICH trial might be due to the inadequate volume reduction (−19%).
Estimating total mortality and asymptotic length of Crangon crangon between 1955 and 2006
Authors: Hufnagl Marc , Temming Axel , Siegel Volker , Tulp Ingrid , Bolle Loes 
Published: February 2010

Abstract
Hufnagl, M., Temming, A., Siegel, V., Tulp, I., and Bolle, L. 2010. Estimating total mortality and asymptotic length of Crangon crangon between 1955 and 2006. – ICES Journal of Marine Science, 67: 875–884. Total mortality (Z, year−1) of southern North Sea brown shrimp (Crangon crangon) was determined as Z = θK, based on the von Bertalanffy length–growth constant (K, year−1) and θ derived from length-based methods. Mortality estimates were based on length frequency distributions obtained from four long-term dataseries (1955–2006): German Demersal Young Fish Survey, Dutch Demersal Fish Survey, and two German Bycatch series (Büsum and East Frisia). Four methods to estimate θ and L∞ were evaluated. Highest total mortality (Z = 8 year−1) was estimated for the early 1990s, and the lowest (Z = 4 year−1) for the 1960s. Accounting for these differences, a median Z rather than mean values was calculated for the whole series, and the value ranged from 5.74 (Ssentongo and Larkin method), through 5.65 (Beverton and Holt method) and 5.64 (Jones and Zalinge method), to 5.35 (length-converted catch curves). Over the whole period, an increase in θ and a decrease in the proportion of shrimps >60 mm in the catch was observed, whereas asymptotic length L∞ remained constant (at 79.3 mm total length).
An expansion of the MSVPA approach for quantifying predator–prey interactions in exploited fish communities
Authors: Garrison Lance P. , Link Jason S. , Kilduff D. Patrick , Cieri Matthew D. , Muffley Brandon , Vaughan Douglas S. , Sharov Alexei , Mahmoudi Behzad , Latour Robert J. 
Published: February 2010

Abstract
Garrison, L. P., Link, J. S., Kilduff, D. P., Cieri, M. D., Muffley, B., Vaughan, D. S., Sharov, A., Mahmoudi, B., and Latour, R. J. 2010. An expansion of the MSVPA approach for quantifying predator–prey interactions in exploited fish communities. – ICES Journal of Marine Science, 67: 856–870. Ecosystem-based fisheries management requires tools to place fish-stock dynamics in the broader context of fishery, predator, and competitive removals. Multispecies virtual population analysis (MSVPA) is an approach to quantifying predator–prey interactions and estimating the rates of predation mortality for exploited fish populations. Here, an extended MSVPA (MSVPA-X) is presented as an alternative to existing MSVPA approaches. Notably, MSVPA-X uses index-tuned VPA methods, applies a more flexible feeding model, and includes an alternative functional feeding response. The MSVPA-X model is applied to a western Atlantic fish community, focusing on Atlantic menhaden and its major fish predators, and a sensitivity analysis of major model parameters is presented. The sensitivity analysis highlights the need for adequate diet sampling. The MSVPA-X represents an improvement over previous approaches by increasing the flexibility to model seasonal and interannual dynamics in the strength of predator–prey interactions. Model results demonstrate that, for menhaden in particular, and forage fish in general, quantifying predation mortality is an important part of effective assessments of forage fish, their predators, and the fisheries of both.
Erythema multiforme, Stevens–Johnson syndrome and toxic epidermal necrolysis: Frozen‐section diagnosis
Authors: HOSAKA Hiroomi , OHTOSHI Shinpei , NAKADA Tokio , IIJIMA Masafumi 
Published: February 2010

AbstractStevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) may be fatal. Although classified by body surface area skin detachment, initial stages of both may present with erythema multiforme (EM)‐like lesions. To diagnose and predict disease activity adequately as early as possible for patients revealing EM‐like lesions, we performed frozen‐section diagnosis. Thirty‐five patients clinically diagnosed as EM, SJS or TEN were biopsied to diagnose and predict disease progression within the initial‐visit day. Half of a histological section taken from a lesion was snap‐frozen and immediately cryostat‐sectioned, acetone‐fixed and stained with hematoxylin–eosin. Specimens were examined with light microscopy for presence of epidermal necrosis. A section from unaffected sites was also examined for 11 patients. Specimens were examined with light microscopy for presence of graft‐versus‐host reaction (GVHR)‐like findings: apoptotic keratinocytes and satellite cell necrosis. Epidermal necrosis was seen in nine patients. Initial diagnosis of the nine was one of overlap SJS‐TEN, four of SJS and four of EM, and final diagnosis of those was one of TEN, one of overlap SJS–TEN, four of SJS and three of EM. Dissociation between initial and final diagnosis was seen in three cases. GVHR‐like findings in the epidermis were observed in two patients finally diagnosed as overlap SJS–TEN and TEN. Frozen sections are useful not only to make a diagnosis of erythema multiforme but to assess a potential to exhibit more aggressive clinical behaviors (SJS or TEN).
Herpetiform pemphigus without anti‐desmoglein 1/3 autoantibodies
Authors: NAKASHIMA Hiroko , FUJIMOTO Manabu , WATANABE Rei , ISHIURA Nobuko , YAMAMOTO Akemi Ishida , HASHIMOTO Takashi , TAMAKI Kunihiko 
Published: February 2010

AbstractWe report a patient with herpetiform pemphigus who was negative for autoantibodies to desmoglein (Dsg)1 or 3. He had erythemas with vesicles lining the margins on the trunk and extremities. Histopathology revealed intraepidermal blister with prominent eosinophil infiltration. Direct and indirect immunofluorescence demonstrated the presence of depositing and circulating immunoglobulin (Ig)G autoantibodies, but no IgA antibodies, to keratinocyte cell surface. Nonetheless, neither anti‐Dsg1 nor Dsg3 antibodies were detected by enzyme‐linked immunosorbent assay. Immunoblotting using human epidermal extracts also showed no reactivity with known intraepidermal or epidermal–dermal junctional substances. Immunoelectronmicroscopy revealed the reactivity on the portion of keratinocyte cell surface but not on the desmosomes. This case suggests that non‐desmoglein antigen on keratinocyte cell surface can be targeted in some patients with this unusual variant of pemphigus.
What’s new in bullous pemphigoid
Authors: UJIIE Hideyuki , SHIBAKI Akihiko , NISHIE Wataru , SHIMIZU Hiroshi 
Published: February 2010

AbstractBullous pemphigoid (BP) is the most common autoimmune blistering disease. BP patients have autoantibodies against type XVII collagen (COL17, also called BP180 or BPAG2), a type II transmembrane protein that spans the lamina lucida and projects into the lamina densa of the epidermal basement membrane. The non‐collagenous 16A domain of COL17 is considered to contain pathogenic epitopes of BP. The transfer of immunoglobulin (Ig)G from BP patients fails to cause blisters on mouse skin probably due to differences between humans and mice in the amino acid sequence of NC16A pathogenic epitope of COL17. Passive transfer of rabbit IgG antibodies against the murine homolog of human COL17 NC16A triggers immune reactions to COL17 in mice, including complement activation, mast cell degranulation and neutrophilic infiltration, resulting in dermal–epidermal separation. Recent studies using COL17‐humanized mice that express human COL17 but lack murine COL17 were the first to demonstrate the pathogenicity of anti‐COL17 human BP IgG autoantibodies in vivo. These new findings provide a greater understanding of BP pathomechanisms and facilitate the development of novel specific and efficient therapeutic strategies for BP.
Bullous pemphigoid as a dermadrome associated with spindle cell carcinoma of the gallbladder
Authors: UMEKOJI Ayano , TSURUTA Daisuke , INOUE Toru , NISHIMORI Takeo , ISHII Masamitsu 
Published: February 2010

AbstractSkin disorders that appear in association with internal malignancies are called dermadromes. Bullous pemphigoid (BP), which is a major autoimmune disease of the skin, is considered to be a dermadrome, although there have been conflicting reports. We report a case of BP that preceded the diagnosis of an internal malignancy. Although we could not detect any malignancies on chest, abdominal or pelvic computer tomography on the first hospital admission, intensive screening on the third admission revealed a gallbladder malignancy. Laparoscopic cholecystectomy was performed. Histopathology showed a spindle cell carcinoma of the gallbladder. To the best of our knowledge, this is the first report of a spindle cell carcinoma of the gallbladder in a patient with BP.
Immune dysregulation of pemphigus in humans and mice
Authors: YOKOYAMA Tomoaki , AMAGAI Masayuki 
Published: February 2010

AbstractPemphigus vulgaris is an autoimmune blistering disease of the skin and mucous membranes that is caused by immunoglobulin (Ig)G autoantibodies against the cadherin‐type adhesion molecule desmoglein (Dsg)3 expressed on stratified epithelial cells. Interaction between antigen‐specific T and B cells, which is selectively achieved through T‐cell receptor/major histocompatibility complex–peptide complex association and subsequently corroborated by co‐stimulatory molecules such as CD40/CD154, is required for production of pathological anti‐desmoglein 3 antibody. Some genetically and environmentally susceptible individuals harbor desmoglein reactive B and T cells, and anti‐desmoglein antibodies were detected in their serum. Analysis of the anti‐desmoglein antibody clones derived from pemphigus patients or pemphigus model mice revealed that pathogenic antibodies mostly react with conformational epitopes on mature form desmogleins, whereas non‐pathogenic ones tend to react with non‐conformational epitopes. Surprisingly, antibodies to the Dsg1 precursor pro‐protein are also cloned from individuals without pemphigus. These observations suggest that active suppression by regulatory cell subsets is dominant in these susceptible individuals. In fact, Dsg‐reactive T‐inducible regulatory type 1 (Tr1) cells are readily detected in healthy carriers of pemphigus‐related human leukocyte antigen haplotypes, but rarely in pemphigus patients. These Tr1 cells can be functionally converted to T‐helper 2‐like cells which secrete interleukin‐2 by inactivation of Foxp3 through antisense oligonucleotides. Thus, delicate balance between self‐reactive lymphocytes and regulatory T cells may be a key element in determining whether individuals produce pathogenic antibodies and develop pemphigus phenotypes or not.
Epidermolysis bullosa acquisita: What’s new?
Authors: ISHII Norito , HAMADA Takahiro , DAINICHI Teruki , KARASHIMA Tadashi , NAKAMA Takekuni , YASUMOTO Shinichiro , ZILLIKENS Detlef , HASHIMOTO Takashi 
Published: February 2010

AbstractType VII collagen is an adhesion molecule of the extracellular matrix in epithelial basement membranes, and the main constituent of anchoring fibrils at the dermal–epidermal junction (DEJ). Autoimmunity against this protein is causing the rare organ‐specific epidermolysis bullosa acquisita (EBA). EBA is a rare acquired, heterogeneous, chronic blistering disease of skin disease of skin and mucous membranes characterized by subepidermal blisters and tissue‐bound as well as circulating autoantibodies to the DEJ. EBA has several distinct clinical presentations with other subepidermal bullous diseases, such as mainly dystrophic epidermolysis bullosa or bullous pemphigoid. The circulating immunoglobulin G autoantibodies for EBA react with a 290‐kDa dermal protein, type VII collagen, as detected by immunoblot analysis using dermal extracts. The pathogenicity of these autoantibodies has been demonstrated by experimental animal models, in which anti‐type VII collagen antibodies injected into a mouse produced an EBA‐like blistering disease in the animal. EBA cases often require high doses of systemic corticosteroids and a variety of immunosuppressants. Although treatment for EBA is frequently difficult and unsatisfactory, some therapeutic success has been reported with colchicine, dapsone, infliximab and i.v. immunoglobulin. In this review, we will focus on recent progress in our understanding of the clinical manifestations, the etiopathogenesis as well as the management of EBA.
Overview of epidermolysis bullosa
Authors: SAWAMURA Daisuke , NAKANO Hajime , MATSUZAKI Yasushi 
Published: February 2010

AbstractEpidermolysis bullosa (EB) is classified into major types – EB simplex (EBS), junctional EB (JEB) and dystrophic EB (DEB) – on the basis of the level of tissue separation within the cutaneous basement membrane zone. Recent advances in research on EB have led to the identification of 10 genes responsible for EB. The Japanese Ministry of Health, Labor and Welfare has designated JEB and DEB, but not EBS, as specified diseases. However, EBS has a lethal variant and should also be registered as a specified disease. In the Third Consensus Meeting on the Diagnosis and Classification of EB held in Vienna in 2007, it was recommended that Kindler syndrome should be classified as a subtype of EB. Corrective gene therapy is the most ideal therapy for EB, but much more research is required before it can be developed and used in clinical practice. Cell‐based therapies using fibroblasts and bone marrow cells have recently attracted considerable attention.
Combustion metamorphism in the Nabi Musa dome: new implications for a mud volcanic origin of the Mottled Zone, Dead Sea area
Authors: Sokol E. , Novikov I. , Zateeva S. , Vapnik Ye. , Shagam R. , Kozmenko O. 
Published: February 2010

ABSTRACTNumerous high‐temperature combustion metamorphic foci within brecciated mainly calcareous sedimentary rocks in the Dead Sea area (the so‐called ‘Mottled Zone’ complexes) have been interpreted as resulting from in situ oxidation and ignition of dispersed organic matter in bituminous chalks. Geological, chemical and petrological data for the Nabi Musa dome, one of 15 Mottled Zone complexes data presented in this paper, suggest an alternative interpretation relating the Mottled Zone complexes to Pliocene–Pleistocene mud volcanism and the associated methane combustion. The geochemistry and mineralogy of sedimentary, combustion metamorphic, localized hydrothermally, altered rocks, and ignition foci marked by ultrahigh temperature (up to 1500 °C) pseudowollastonite–rankinite–nagelschmidtite‐bearing paralava, indicate that Nabi Musa is a fossil mud volcano, comprising a large diatreme edifice with brecciated sedimentary rocks in its main feeder. The mud volcanic event mobilized sediments of underlying Cretaceous strata from depths of at least 0.8 km, and the eruption was driven by hydrocarbon gases (predominantly methane), with gas flaming causing local combustion metamorphism. Besides ultrahigh temperature combustion metamorphic processes, ejected sedimentary rocks were subsequently altered by low‐temperature hydrothermal fluids from various sources, which produced specific rock compositions with local enrichments in Mg, Na, Cl and B. Later, carbonation almost completely replaced the original smectite‐bearing parent mud and preserved the edifice from erosion. The proposed mud‐volcanic origin of the Mottled Zone complexes may have implications for gas prospecting in the Levantine basin.
Hormonal and metabolic effects of morning or evening dosing of the dipeptidyl peptidase IV inhibitor vildagliptin in patients with type 2 diabetes
Authors: He Yan‐Ling , Valencia Jessica , Zhang Yiming , Schwartz Sherwyn L. , Ligueros‐Saylan Monica , Foley James , Dole William P. 
Published: February 2010

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT • Vildagliptin is an orally active, potent inhibitor of dipeptidyl peptidase IV and was developed for the treatment of type 2 diabetes.• In clinical trials, once or twice daily dosing with vildagliptin (up to 100 mg day−1) has been shown to reduce endogenous glucose production and fasting plasma glucose in patients with type 2 diabetes.• The comparative efficacy of vildagliptin under a morning vs. evening dosing regimen has not previously been determined. WHAT THIS STUDY ADDS • Once daily dosing with vildagliptin 100 mg for 28 days improved glycaemic control in patients with type 2 diabetes independent of whether vildagliptin was administered in the morning or evening.• Morning or evening dosing with vildagliptin had similar effects on 24 h glycaemic control and plasma concentrations of the hormones insulin, glucagon and glucagon‐like peptide 1.AIMThis randomized, double‐blind, crossover study compared post‐prandial hormonal and metabolic effects of vildagliptin, (an oral, potent, selective inhibitor of dipeptidyl peptidase IV [DPP‐4]) administered morning or evening in patients with type 2 diabetes.METHODSForty‐eight patients were randomized to once daily vildagliptin 100 mg administered before breakfast or before dinner for 28 days then crossed over to the other dosing regimen. Blood was sampled frequently after each dose at baseline (day −1) and on days 28 and 56 to assess pharmacodynamic parameters.RESULTSVildagliptin inhibited DPP‐4 activity (>80% for 15.5 h post‐dose), and increased active glucagon‐like peptide‐1 compared with placebo. Both regimens reduced total glucose exposure compared with placebo (area under the 0–24 h effect–time curve [AUE(0,24 h)]: morning −467 mg dl−1 h, P= 0.014; evening −574 mg dl−1 h, P= 0.003) with no difference between regimens (P= 0.430). Reductions in daytime glucose exposure (AUE(0,10.5 h)) were similar between regimens. Reduction in night‐time exposure (AUE(10.5,24 h) was greater with evening than morning dosing (−336 vs.−218 mg dl−1 h, P= 0.192). Only evening dosing significantly reduced fasting plasma glucose (−13 mg dl−1, P= 0.032) compared with placebo. Insulin exposure was greater with evening dosing (evening 407 µU ml−1 h; morning 354 µU ml−1 h, P= 0.050).CONCLUSIONSBoth morning and evening dosing of once daily vildagliptin 100 mg significantly reduced post‐prandial glucose in patients with type 2 diabetes; only evening dosing significantly decreased fasting plasma glucose. Although evening dosing with vildagliptin 100 mg tended to decrease night‐time glucose exposure more than morning dosing, both regimens were equally effective in reducing 24 h mean glucose exposure (AUE(0,24 h)) in patients with type 2 diabetes.