bluuebunny/crossref_metadata_2025_split huggingface dataset:
Myrothecium roridum Leaf Spot and Stem Canker on Watermelon in the Southern Great Plains: Possible Factors for Its Outbreak
Authors: Bruton Benny D. , Fish Wayne W. 
Published: February 2012

In 2010, a foliar and stem-lesion disease was observed for the first time in Oklahoma causing moderate to severe defoliation. Using microscopic examination, the physical features of the fungus were consistent with Myrothecium roridum. There was a wide range of susceptibility among watermelon cultivars in the field indicating a moderately high level of resistance to Myrothecium leaf spot in some cultivars. In greenhouse inoculation experiments, cantaloupe, honeydew, cucumber, squash, and watermelon were all susceptible to the fungus with cantaloupe and honeydew being the most susceptible and watermelon the most resistant. Furthermore, greenhouse inoculations supported the field observations as differential resistance was exhibited among the watermelon cultivars as well as the cucurbit types. Although cantaloupe was most susceptible to the foliar phase of this disease, watermelon was most susceptible to the fruit-rot phase. Natural infection of watermelon fruit has never been reported. Accepted for publication 15 December 2011. Published 30 January 2012.
Local structures of mesoporous bioactive glasses and their surface alterations
in vitro
: inferences from solid-state nuclear magnetic resonance
Authors: Gunawidjaja Philips N. , Mathew Renny , Lo Andy Y. H. , Izquierdo-Barba Isabel , García Ana , Arcos Daniel , Vallet-Regí María , Edén Mattias 
Published: February 2012

We review the benefits of using
29
Si and
1
H magic angle spinning (MAS) nuclear magnetic resonance (NMR) spectroscopy for probing the local structures of both bulk and surface portions of mesoporous bioactive glasses (MBGs) of the CaO–SiO
2
−(P
2
O
5
) system. These mesoporous materials exhibit an ordered pore arrangement, and are promising candidates for improved bone and tooth implants. We discuss experimental MAS NMR results from three MBGs displaying different Ca, Si and P contents: the
29
Si NMR spectra were recorded either directly by employing radio-frequency pulses to
29
Si, or by magnetization transfers from neighbouring protons using cross polarization, thereby providing quantitative information about the silicate speciation present in the pore wall and at the MBG surface, respectively. The surface modifications were monitored for the three MBGs during their immersion in a simulated body fluid (SBF) for intervals between 30 min and one week. The results were formulated as a reaction sequence describing the interconversions between the distinct silicate species. We generally observed a depletion of Ca
2+
ions at the MBG surface, and a minor condensation of the silicate-surface network over one week of SBF soaking.
Overexpression of ADP‐ribosylation factor 1 in human gastric carcinoma and its clinicopathological significance
Authors: Tsai Ming‐Ming , Lin Paul Y. , Cheng Wan‐Li , Tsai Chung‐Ying , Chi Hsiang‐Cheng , Chen Cheng‐Yi , Tseng Yi‐Hsin , Cheng Yi‐Fen , Chen Chi‐De , Liang Ying , Liao Chia‐Jung , Wu Sheng‐Ming , Lin Yang‐Hsiang , Chung I‐Hsiao , Wang Chia‐Siu , Lin Kwang‐Huei 
Published: February 2012

Gastric cancer is the sixth leading cause of cancer‐related death in Taiwan, and the identification of related factors is essential to increase patient survival. ADP‐ribosylation factor 1 (ARF1) was initially identified using 2‐D electrophoresis combined with MALDI–time‐of‐flight mass spectrometry. ADP‐ribosylation factor 1 belongs to the Ras superfamily or GTP‐binding protein family and has been shown to enhance cell proliferation. In the current study, we evaluated the potential of ARF1 as a biomarker for gastric cancer detection. ADP‐ribosylation factor 1 mRNA was upregulated in tumor tissues (compared with adjacent non‐tumor tissues, n = 55) in approximately 67.2% of gastric cancer patients. Expression of ARF1 protein was additionally observed using Western blot and immunohistochemistry (IHC) analyses. The clinicopathological correlations of ARF1 were further evaluated. Elevated ARF1 expression was strongly correlated with lymph node metastasis (P = 0.008), serosal invasion (P = 0.046), lymphatic invasion (P = 0.035), and pathological staging (P = 0.010). Moreover, the 5‐year survival rate for the lower ARF1 expression group (n = 50; IHC score < 90) was higher than that of the higher expression group (n = 60; IHC score ≥ 90) (P = 0.0228, log–rank test). To establish the specific function of ARF1 in human gastric cancer, isogenic ARF1‐overexpressing cell lines were prepared. Our results showed that ARF1‐overexpressing clones display enhanced cell proliferation, migration, and invasion. Furthermore, ARF1‐overexpression might contribute to poor prognosis of patients. These findings collectively support the utility of ARF1 as a novel prognostic marker for gastric cancer and its role in cell invasion. Cancer Sci 2012; 103: 1136–1144)
Decrease in the oral bioavailability of dabigatran etexilate after co‐medication with rifampicin
Authors: Härtter Sebastian , Koenen‐Bergmann Michael , Sharma Ashish , Nehmiz Gerhard , Lemke Ute , Timmer Wolfgang , Reilly Paul A. 
Published: February 2012

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT• Dabigatran etexilate is an oral prodrug that is rapidly converted to dabigatran, a direct and reversible thrombin inhibitor.• Dabigatran etexilate and dabigatran are not metabolized by the cytochrome P450 system, and dabigatran does not affect the metabolism of other drugs that utilize this system, leading to a low potential for drug–drug interactions.• Dabigatran etexilate, but not dabigatran, is a P‐glycoprotein (P‐gp) substrate, and the bioavailability of dabigatran may be altered by P‐gp inhibitors or inducers.WHAT THIS STUDY ADDS• Administration of rifampicin (a strong P‐gp inducer) for 7 days before a single dose of dabigatran etexilate resulted in a significant reduction in the bioavailability of dabigatran compared with administration of dabigatran etexilate alone.• Within 7 days following the cessation of rifampicin administration, the bioavailability of dabigatran returned almost to baseline values.• Rifampicin is not recommended for use with dabigatran etexilate because of the potential for reduced systemic exposure to dabigatran.AIMS This study examined the effects of the CYP3A/P‐glycoprotein inducer, rifampicin, on the pharmacokinetics of dabigatran following oral administration of the prodrug, dabigatran etexilate.METHODS This was an open‐label, fixed‐sequence, four‐period study in healthy volunteers. Subjects received a single dose of dabigatran etexilate 150 mg on day 1, rifampicin 600 mg once daily on days 2–8, and single doses of dabigatran etexilate on days 9, 16 and 23.RESULTS Twenty‐four subjects were treated, of whom 22 received all treatments. Relative to the reference (single dose of dabigatran etexilate alone; treatment A), administration of dabigatran etexilate following 7 days of rifampicin (treatment B) decreased the geometric mean (gMean) area under the concentration–time curve (AUC0–∞) and maximal plasma concentration (Cmax) of total dabigatran by 67 and 65.5%, respectively. The time to peak and the terminal half‐life were not affected. The gMean ratio for the primary comparison (treatment B vs. treatment A) was 33.0% (90% confidence interval 26.5, 41.2%) for AUC0–∞ and 34.5% (90% confidence interval 26.9, 44.1%) for Cmax, indicating a significant effect on total dabigatran exposure (total pharmacologically active dabigatran represents the sum of nonconjugated dabigatran and dabigatran glucuronide). After a 7 day (treatment C) or 14 day washout (treatment D), the AUC0–∞ and Cmax of dabigatran were reduced by 18 and 20%, and by 15 and 20%, respectively, compared with treatment A, which was considered not clinically relevant. The overall safety profile of all treatments was good.CONCLUSIONS Administration of rifampicin for 7 days resulted in a significant reduction in the bioavailability of dabigatran, which returned almost to baseline after 7 days washout.
How I manage aplastic anaemia in children
Authors: Samarasinghe Sujith , Webb David K. H. 
Published: February 2012

SummaryAplastic anaemia (AA) is a rare heterogeneous condition in children. 15–20% of cases are constitutional and correct diagnosis of these inherited causes of AA is important for appropriate management. For idiopathic severe aplastic anaemia, a matched sibling donor (MSD) haematopoietic stem cell transplant (HSCT) is the treatment of choice. If a MSD is not available, the options include immunosuppressive therapy (IST) or unrelated donor HSCT. IST with horse anti‐thymocyte globulin (ATG) is superior to rabbit ATG and has good long‐term results. In contrast, IST with rabbit ATG has an overall response of only 30–40%. Due to improvements in outcome over the last two decades in matched unrelated donor (MUD) HSCT, results are now similar to that of MSD HSCT. The decision to proceed with IST with ATG or MUD HSCT will depend on the likelihood of finding a MUD and the differing risks and benefits that each therapy provides.
The effect of gestation and fetal mismatching on the development of autoimmune diabetes in non-obese diabetic mice
Authors: Adler K , Krause S , Fuchs Y F , Foertsch K , Ziegler A-G , Bonifacio E 
Published: February 2012

Summary
The impact of gestation and fetal–maternal interactions on pre-existent autoimmune beta cell destruction is widely unknown. The aim of this study was to investigate the influence of gestation per se and fetal mismatching on the onset of autoimmune diabetes in female non-obese diabetic (NOD) mice. We examined cumulative diabetes frequencies of NOD dams mated to syngeneic NOD, haploidentical CByB6F1/J and fully mismatched C57BL/6J male mice. Pregnancy from NOD males neither increased nor accelerated the diabetes onset of NOD dams (71% by age 28 weeks) compared to unmated female NOD mice (81% by age 28 weeks; P = 0·38). In contrast, delayed diabetes onset was observed when NOD dams were mated at 10 weeks of age with major histocompatibility complex (MHC) haploidentical CByB6F1/J male mice (38% at age 28 weeks; P = 0·01). Mating with fully MHC mismatched C57BL/6J male mice (72% diabetes by age 28 weeks; P = 0·22) or mating with the haploidentical males at the later time-point of age 13 weeks (64% versus 91% in unmated litter-matched controls; P = 0·13) did not delay diabetes significantly in NOD females. Because infusion of haploidentical male mouse splenocytes was found previously to prevent diabetes in NOD mice we looked for, but found no evidence of, persistent chimeric lymphocytes from haploidentical paternal origin within the dams' splenocytes. Gestation per se appears to have no aggravating or ameliorating effects on pre-existent autoimmune beta cell destruction, but pregnancy from MHC partially mismatched males delays diabetes onset in female NOD mice.
Cordycepin as a sensitizer to tumour necrosis factor (TNF)-α-induced apoptosis through eukaryotic translation initiation factor 2α (eIF2α)- and mammalian target of rapamycin complex 1 (mTORC1)-mediated inhibition of nuclear factor (NF)-κB
Authors: Kadomatsu M , Nakajima S , Kato H , Gu L , Chi Y , Yao J , Kitamura M 
Published: February 2012

SummaryCordycepin (3′-deoxyadenosine) is one of the major bioactive substances produced by Cordyceps militaris, a traditional medicinal mushroom. Cordycepin possesses several biological activities, including both pro-apoptotic and anti-apoptotic properties. In the present report, we investigated an effect of cordycepin on the survival of cells exposed to tumour necrosis factor (TNF)-α. We found that subtoxic doses of cordycepin increased susceptibility of cells to TNF-α-induced apoptosis. It was associated with suppression of nuclear factor-κB (NF-κB), a major prosurvival component involved in TNF-α signalling. The adenosine transporter and A3 adenosine receptor, but not A1 and A2 adenosine receptors, mediated both anti-NF-κB and pro-apoptotic effects. We found that cordycepin had the potential to phosphorylate eukaryotic translation initiation factor 2α (eIF2α) and that activation of eIF2α mimicked the suppressive effect of cordycepin on the NF-κB pathway. Furthermore, activation of eIF2α sensitized cells to TNF-α-induced apoptosis. To identify molecular events downstream of eIF2α, the role of mammalian target of rapamycin complex 1 (mTORC1) was examined. Selective activation of 3eIF2α, as well as treatment with cordycepin, caused phosphorylation of mTORC1. Rapamycin, an inhibitor of mTORC1, significantly reversed the suppressive effects of eIF2α on NF-κB. These results suggest that cordycepin sensitizes cells to TNF-α-induced apoptosis, at least in part, via induction of the eIF2α–mTORC1 pathway and consequent suppression of NF-κB.
Sex cells in changing environments: can organisms adjust the physiological function of gametes to different temperatures?
Authors: Adriaenssens Bart , van Damme Raoul , Seebacher Frank , Wilson Robbie S. 
Published: February 2012

AbstractOver the past decade, hundreds of studies have examined the abilities of whole organisms to modify their physiology and behaviour in response to environmental temperature changes; despite this, virtually nothing is known about the ability of sex cells to adjust to different temperature conditions. In fact, a recent meta‐analysis based on studies of 309 species and 112 physiological and ecological traits found no studies examining the influence of temperature on gamete function. Because sex cells play a critical role in the adaptation and persistence of species, this represents a severe oversight in physiological studies of thermal adaptation. Our study examines whether sex cells can respond phenotypically to variation in the thermal environment that is experienced by the whole‐organism. Specifically, we studied the thermal dependence of sperm swimming and the critical thermal limits of sperm cells in males of the poeciliid fish, Gambusia holbrooki. This species is well known for its ability to modify physiological function and maintains burst and sustained swimming performance and mating ability across a wide range of thermal conditions. In contrast, we found that sperm cells from male G. holbrooki did not adjust their physiological function as predicted by adaptive models. After acclimation of adult males to cool or warm temperatures, we found that the critical thermal limits of sperm function remained unchanged, as did the effect of temperature on sperm swimming performance. However, warm‐acclimated fish had sperm with higher swimming speeds across all temperatures. The absence of phenotypic changes in the critical thermal limits of sperm or thermal dependence of sperm swimming performance is surprising given that whole‐organism traits in G. holbrooki generally show improved performance after exposure to novel environments. As such an inability to thermally adjust gamete function may be widespread among other organisms, we urge biologists to investigate the generality of this result.
Climate effects on size‐at‐age: growth in warming waters compensates for earlier maturity in an exploited marine fish
Authors: Neuheimer Anna B. , Grønkjær Peter 
Published: February 2012

AbstractOver the past 3 decades, North Sea Atlantic cod (Gadus morhua) have exhibited variable length‐at‐age along with declines in spawning stock biomass and timing of maturity. Multiple factors affecting growth and development in fish acted on this economically important stock over the same period including warming waters and an intensive fishery. Here, we employ North Sea cod as a model population, exploring how a physiologically relevant temperature metric (the growing degree‐day, GDD; °C day) can be used to compare year‐classes on a physiologically relevant time‐scale, disentangling influences of climate (thermal history) on observed length‐at‐age trends. We conclude that the trends in North Sea cod length‐at‐age observed during the last three decades can be explained by a combination of temperature‐dependent growth increases and a trend toward earlier maturation, the latter likely induced by the intensive fishing pressure, and possibly evidence of fisheries‐induced evolution.
The value of immunohistochemistry for CD14, CD123, CD33, myeloperoxidase and CD68R in the diagnosis of acute and chronic myelomonocytic leukaemias
Authors: Rollins‐Raval Marian A , Roth Christine G 
Published: February 2012

Rollins‐Raval M A & Roth C G  (2012) Histopathology 60, 933–942The value of immunohistochemistry for CD14, CD123, CD33, myeloperoxidase and CD68R in the diagnosis of acute and chronic myelomonocytic leukaemiasAims:  In the absence of adequate aspirate films and touch imprints, distinction of chronic myelomonocytic leukaemia (CMML) from acute myeloid leukaemia with monocytic differentiation (Mo‐AML) may be difficult solely on the basis of bone marrow biopsy morphological features. The aim of this study was to evaluate the diagnostic utility of a novel immunohistochemical panel for the diagnosis of acute and chronic myelomonocytic leukaemias in bone marrow biopsies.Methods and results:  Immunohistochemical labelling for CD14, CD123, CD33, myeloperoxidase (MPO) and CD68R was assessed in 49 myeloid neoplasms with monocytic differentiation (24 CMMLs and 25 Mo‐AMLs) and compared with that of 15 non‐monocytic acute myeloid leukaemias (NM‐AMLs) and 17 non‐neoplastic controls. More than 20% CD14 immunohistochemistry (IHC)+ cells were seen only in Mo‐AMLs and CMMLs, although Mo‐AMLs showed wide variability and overlapped with other categories. More than 20% CD68R IHC+ cells had the highest sensitivity and specificity for Mo‐AML. Discrepant MPO–/CD33+ expression was specific for Mo‐AML but insensitive. A subset of blasts in Mo‐AMLs and NM‐AMLs were weakly CD123+.Conclusions:  A significantly increased number of CD14+ cells raises the possibility of a myelomonocytic neoplasm but does not distinguish between CMML and Mo‐AML. Significantly increased numbers of CD68R IHC+ cells and a discrepant MPO–/CD33+ staining pattern are specific for Mo‐AML but are best utilized in a comprehensive panel.
Poorly differentiated oncocytic thyroid carcinoma – diagnostic implications and outcome
Authors: Dettmer Matthias , Schmitt Anja , Steinert Hans , Moch Holger , Komminoth Paul , Perren Aurel 
Published: February 2012

Dettmer M, Schmitt A, Steinert H, Moch H, Komminoth P & Perren A  (2012) Histopathology 60, 1045–1051Poorly differentiated oncocytic thyroid carcinoma – diagnostic implications and outcomeAims:  Poorly differentiated thyroid carcinomas (PDTC) are an ongoing diagnostic challenge. Although the Turin consensus criteria for PDTC excluded consideration of oncocytic tumours, the World Health Organization (WHO) classification does recognise an oncocytic variant of conventional PDTC. The aims of this study were to establish whether the Turin criteria can be applied to oncocytic PDTC, and to determine if there are prognostic differences between conventional and oncocytic PDTC.Methods and results:  We applied the Turin criteria to 129 thyroid carcinomas. We identified 18 oncocytic PDTC and 16 conventional PDTC. Kaplan–Meier analysis revealed a significantly worse outcome for oncocytic PDTC with regard to overall and tumour‐specific survival but no difference for relapse‐free survival, all of which were confirmed by multivariate analysis. There was no association of survival with gender, age or tumour stage.Conclusions:  The Turin criteria can be applied to oncocytic PDTC and patients with this variant have a decreased survival using conventional radioiodine treatment compared to conventional PDTC and might therefore be candidates for novel treatment modalities.
Nanoparticle tracking analysis monitors microvesicle and exosome secretion from immune cells
Authors: Soo Chin Y. , Song Yaqiong , Zheng Ying , Campbell Elaine C. , Riches Andrew C. , Gunn‐Moore Frank , Powis Simon J. 
Published: February 2012

SummaryNanoparticle tracking analysis permits the determination of both the size distribution and relative concentration of microvesicles, including exosomes, in the supernatants of cultured cells and biological fluids. We have studied the release of microvesicles from the human lymphoblastoid T‐cell lines Jurkat and CEM. Unstimulated, both cell lines release microvesicles in the size range 70–90 nm, which can be depleted from the supernatant by ultracentrifugation at 100 000 g, and by anti‐CD45 magnetic beads, and which by immunoblotting also contain the exosome‐associated proteins Alix and Tsg101. Incubation with known potentiators of exosome release, the ionophores monensin and A23187, resulted in a significant increase in microvesicle release that was both time and concentration dependent. Mass spectrometric analysis of proteins isolated from ultracentrifuged supernatants of A23187‐treated cells revealed the presence of exosome‐associated proteins including heat‐shock protein 90, tubulin, elongation factor α1, actin and glyceraldehyde 3‐phosphate dehydrogenase. Additionally, treatment of peripheral blood monocyte‐derived dendritic cells with bacterial lipopolysaccharide displayed an increase in secreted microvesicles. Consequently, nanoparticle tracking analysis can be effectively applied to monitor microvesicle release from cells of the immune system.
T‐cell receptor retrogenic mice: a rapid, flexible alternative to T‐cell receptor transgenic mice
Authors: Bettini Matthew L. , Bettini Maria , Vignali Dario A. A. 
Published: February 2012

SummaryThe T‐cell receptor (TCR) is unique in its complexity. It determines not only positive (life) and negative (death) selection in the thymus, but also mediates proliferation, anergy, differentiation, cytotoxicity and cytokine production in the periphery. Through its association with six CD3 signalling chains (εγ, δε and ζζ), the TCR is capable of recognizing an extensive variety of antigenic peptides, from both pathogens and self‐antigens, and translating these interactions into multiple signalling pathways that mediate diverse T‐cell developmental and functional responses. The analysis of TCR biology has been revolutionized by the development of TCR transgenic mice, which express a single clonotypic T‐cell population, with diverse specificities and genetic backgrounds. However, they are time consuming to generate and characterize, limiting the analysis of large numbers of TCR over a short period of time in multiple genetic backgrounds. The recent development of TCR retrogenic technology resolves these limitations and could in time have a similarly important impact on our understanding of T‐cell development and function. In this review, we will discuss the advantages and limitations of retrogenic technology compared with the generation and use of TCR transgenic mice for studying all aspects of T‐cell biology.