bluuebunny/crossref_metadata_2025_split huggingface dataset:
Seroprevalence of occult hepatitis B among Egyptian paediatric hepatitis C cancer patients
Authors: Raouf H. E. , Yassin A. S. , Megahed S. A. , Ashour M. S. , Mansour T. M. 
Published: April 2014

SummaryOccult hepatitis B infection is characterized by the presence of hepatitis B virus (HBV) DNA in the serum in the absence of hepatitis B surface antigen (HBsAg). Prevalence of hepatitis C virus (HCV) infections in Egypt is among the highest in the world. In this study, we aim at analysing the rates of occult HBV infections among HCV paediatric cancer patients in Egypt. The prevalence of occult HBV was assessed in two groups of paediatric cancer patients (HCV positive and HCV negative), in addition to a third group of paediatric noncancer patients, which was used as a general control. All groups were negative for HBsAg and positive for HCV antibody. HBV DNA was detected by nested PCR and real‐time PCR. HCV was detected by real‐time PCR. Sequencing was carried out in order to determine HBV genotypes to all HBV patients as well as to detect any mutation that might be responsible for the occult phenotype. Occult hepatitis B infection was observed in neither the non‐HCV paediatric cancer patients nor the paediatric noncancer patients but was found in 31% of the HCV‐positive paediatric cancer patients. All the detected HBV patients belonged to HBV genotype D, and mutations were found in the surface genome of HBV leading to occult HBV. Occult HBV infection seems to be relatively frequent in HCV‐positive paediatric cancer patients, indicating that HBsAg negativity is not sufficient to completely exclude HBV infection. These findings emphasize the importance of considering occult HBV infection in HCV‐positive paediatric cancer patients especially in endemic areas as Egypt.
Transcriptional profiling of human gingival fibroblasts in response to multi‐species in vitro subgingival biofilms
Authors: Belibasakis G.N. , Bao K. , Bostanci N. 
Published: April 2014

SummaryPeriodontitis is an infectious inflammatory disease that destroys the tooth‐supporting tissues. It is initiated by complex subgingival biofilms, triggering an inflammatory response by the juxtaposed gingival tissue. The range of transcriptional events initiated in the gingiva following biofilm challenge is not fully elucidated. By employing gene microarray technology, this study aimed to characterize the overall transcriptional changes (more than two‐fold regulation) of cultured human gingival fibroblasts in response to a 10‐species in vitro subgingival biofilm model (BF), over a challenge period of 6 h. The relative involvement of the three ‘red complex’ species in these transcriptional events was evaluated by omitting these species from the biofilm composition (BF‐RC). When compared with the unchallenged control, challenge with BF and BF‐RC differentially regulated 386 and 428 genes, respectively, with an overlap of 52–75%. Interestingly, the expression of only three genes was significantly different between the BF and BF‐RC challenged groups. There was also a strong overlap of the affected signalling pathways and gene ontology processes. These signalling pathways involved primarily the immune response, and included toll‐like receptors, interleukin‐1, interleukin‐17 and heat‐shock proteins 60 and 70. In conclusion, subgingival biofilms elicited a large number of transcriptional changes in gingival fibroblasts, while the presence of the ‘red complex’ in the biofilm did not yield any substantial differences. These findings show a uniform ‘non‐specific’ transcriptional response of host cells to subgingival biofilms, and denote that redundancies may exist in the virulence properties of individual bacterial species within a polymicrobial biofilm community.
Evaluation of a semi‐controlled test as a selection tool for frost tolerance in durum wheat (Triticum durum)
Authors: Sieber Alisa‐Naomi , Würschum Tobias , Longin Carl Friedrich Horst 
Published: April 2014

AbstractMost durum wheat (Triticum durum) varieties possess only low winter hardiness due to their frost susceptibility. In North America and Central Europe, durum wheat is therefore typically sown in spring to circumvent the local winter conditions. However, the yield potential of durum in these regions could be much better exploited if durum varieties with increased frost tolerance were available, which could be sown in autumn. A factor limiting breeding for increased frost tolerance is the variation in the occurrence of frost stress across years. The ‘Weihenstephaner Auswinterungsanlage’ is a semi‐controlled test that exposes the plants to all weather conditions. Snow coverage of the plants, serving as frost protection, is prevented by the movable glass lid of the semi‐controlled test. In this study, different scorings for frost tolerance based on this semi‐controlled test were evaluated and compared with frost tolerance data in the field. Our results illustrate the potential of the ‘Weihenstephaner Auswinterungsanlage’ as an indirect selection tool for frost tolerance in durum breeding programmes, especially when regular frost tolerance data from the field are not available.
The Endometrium of Cycling Cows Contains Populations of Putative Mesenchymal Progenitor Cells
Authors: Cabezas J , Lara E , Pacha P , Rojas D , Veraguas D , Saravia F , Rodríguez‐Alvarez L , Castro FO 
Published: April 2014

ContentsEndometrial stem cells have been identified in humans, mice and pigs. This study was designed to determine whether the uterine endometrium of cycling cows contains such cells, to identify markers of stemness and ultimately to isolate putative stem/progenitor cell and evaluate their capability to differentiate into mesodermal derivatives. Uteri from healthy cows in the early (days 1–5) and late luteal phases (days 13–18) of the oestrous cycle were collected. Total RNA and proteins were isolated and searched for gene markers of embryonic (OCT4, NANOG, SOX2) and mesenchymal (CD44, STAT3, CD‐117) stem cells and for protein markers (Oct4, Sox2, Cd44) in Western blots or immunostaining of paraffin‐embedded tissue. Primary cell cultures were isolated; characterized in terms of morphology, colony formation and gene/protein expression; and induced osteogenic and chondrogenic differentiation. We identified expression of embryonic (OCT4 and SOX2, but not NANOG) and mesenchymal (STAT3, CD44 and c‐KIT) gene markers in the endometrium of cycling cows and the encoded proteins (Oct4, Sox2 and Cd44) in both stages of the oestrous cycle. Derived cell lines displayed essentially the same gene expression pattern; however, at the protein level, Oct4 was not detected. No clear influence of the stage of the oestrous cycle was found. Cell lines from late luteal phase displayed osteogenic and chondrogenic differentiation potential upon chemical stimulation. In this research, we demonstrated the presence of mesenchymal progenitor cell populations of apparently mesenchymal origin in the endometrium of cycling cows, in both the early and late phases of the oestrous cycle. The cells isolated from the late luteal phase were more acquiescent to differentiate into mesodermal derivatives than cells in the early luteal phase. Our findings might have implications for the understanding of uterine stem cell biology in cows and other farm animal species.
Semiparametric Time Series Models with Log‐concave Innovations: Maximum Likelihood Estimation and its Consistency
Authors: Chen Yining 
Published: April 2014

AbstractWe study semiparametric time series models with innovations following a log‐concave distribution. We propose a general maximum likelihood framework that allows us to estimate simultaneously the parameters of the model and the density of the innovations. This framework can be easily adapted to many well‐known models, including autoregressive moving average (ARMA), generalized autoregressive conditionally heteroscedastic (GARCH), and ARMA‐GARCH models. Furthermore, we show that the estimator under our new framework is consistent in both ARMA and ARMA‐GARCH settings. We demonstrate its finite sample performance via a thorough simulation study and apply it to model the daily log‐return of the FTSE 100 index.
Technologies for increasing carbon storage in soil to mitigate climate change
Authors: Whitmore A. P. , Kirk G. J. D. , Rawlins B. G. 
Published: April 2014

AbstractMeans to enhance storage of carbon in soil or avoid its loss from soil are discussed and examined from the viewpoint of policy. In particular, technologies that have until now received little attention are assessed. The main means by which soil carbon might be increased are first listed. These are the following: (i) increasing the rate of input of organic matter; (ii) decreasing the rate of its decomposition by biological or chemical means; (iii) increasing the rate of its stabilization by physico‐chemical protection within aggregates and organo‐mineral complexes; and (iv) increasing the depth or more correctly the total soil volume sequestering carbon at maximum rate. Immediate gains in carbon storage might be made by switching to more perennial crops, especially grasses that, as a result of breeding, are able to put more carbon into soil. In the longer term, targets for research such as understanding the role of enzymes in carbon turnover and the exploitation of the capacity in subsoils are suggested. Increased fixation of CO2 as inorganic carbonate in soils by application of silicate wastes may have some role.
Association of IGF1R polymorphisms with the development of HBV‐related hepatocellular carcinoma
Authors: Xie H.‐Y. , Xing C.‐Y. , Wei B.‐J. , Xu X. , Wu J. , Chen L.‐M. , Cao G.‐Q. , Chen H. , Chen K.‐J. , Yin S.‐Y. , Wu L.‐M. , Zhou L. , Zheng S.‐S. 
Published: April 2014

AbstractAlthough the involvement of insulin‐like signaling in cancer has been well documented in various types of cancers, the association between the genetic variants in the insulin‐like signaling and the development of hepatitis B virus (HBV)‐related hepatocellular carcinoma (HCC) remains unclear. In this study, a total of 498 individuals including 173 HBV related cirrhosis patients, 171 HBV‐related HCC patients, and 154 healthy controls were enrolled. Sixteen single nucleotide polymorphisms (SNPs) in IGF1, IGF2, IGF1R and IGF2R have been genotyped by employing SNaPshot assays. We found A/A genotype at rs3743251 of IGF1R was negatively associated with HBV related HCC [odds ratio (OR) = 0.38, 95% confidence interval (CI) = 0.20–0.72, P = 0.037]; A/G genotype decreased the risk of portal vein thrombosis (OR = 0.38, 95%CI = 0.18–0.82, P = 0.01). These results indicate that rs3743251 polymorphism in IGF1R is associated with the susceptibility of HBV‐related HCC.
Somatic mutation in acute myelogenous leukemia cells imitate novel germline HLA‐A allele: a case report
Authors: Mrazek F. , Onderkova J. , Szotkowski T. , Königova N. , Ambruzova Z. , Raida L. 
Published: April 2014

AbstractA somatic mutation of the human leukocyte antigen (HLA)‐A gene revealed in tumour cells of acute myelogenous leukemia (AML) is described. A patient with AML and her siblings were routinely typed for HLA in order to find a suitable donor for haematopoietic stem cell transplantation. Sequencing‐based typing of the initial patient's sample characterized by high proportion of blasts revealed unknown G/A exchange at position 781 of the HLA‐A gene (exon 4) associated with HLA‐A*02:01 allele. Importantly, this G781A variant was completely absent in the patient's remission sample obtained after the clearance of blasts. Our results are a reminder that HLA mutations in tumour cells may interfere with routine HLA typing and should always be considered, namely, in patients with haematological malignancies.
The CTLA4 +49 A/G (rs231775) polymorphism influences susceptibility to SLE in South Indian Tamils
Authors: Devaraju P. , Gulati R. , Singh B. K. , Mithun C. B. , Negi V. S. 
Published: April 2014

AbstractSystemic lupus erythematosus (SLE) is a prototype autoimmune disease with complex etiology. Loss of immune tolerance and synthesis of autoantibodies against nuclear antigens contributes to the disease. Genetic aberrations disrupting the functions of immune regulatory receptors may facilitate the development of autoimmune diseases. Cytotoxic T‐lymphocyte antigen 4 (CTLA4) is an inhibitory receptor for T cells and this study was carried out to analyze the influence of CTLA4 +49A/G (rs231775) polymorphism on susceptibility to SLE in ethnic Tamils. Three hundred SLE patients and 460 age and sex similar, ethnicity‐matched controls were screened for the +49 A/G polymorphism by real time polymerase chain reaction (PCR). The wild allele (A) frequency in controls and cases was 63% and 47%, respectively. The presence of heterozygous (AG) and homozygous mutant (GG) genotype was associated with a significant risk to develop SLE (P = 0.0001, OR‐2.29, 95% confidence interval (CI), 1.6–3.3) and (P = 0.0001, OR‐4.3, 95% CI, 2.8–6.99). The frequency of mutant allele (G) in patients was also significantly associated with SLE (P = 0.0001, OR‐1.9, 95% CI, 1.5–2.4). However, this polymorphism did not influence the clinical or serological phenotypes in our study. Therefore the CTLA4 +49 A/G polymorphism is a potential genetic risk factor for lupus susceptibility in South Indian Tamils, but does not appear to influence either the clinical or serological phenotype.
Inequality, Saving and Global Imbalances: A New Theory with Evidence from OECD and Asian Countries
Authors: Gu Xinhua , Dong Baomin , Huang Bihong 
Published: April 2014

AbstractGlobal imbalances are attributable to savings deficiency in some economies and savings glut in others. The recent global crisis has triggered widespread social conflict over income inequality. The inequality‐saving link has again become a pressing issue needing serious attention. We present a new theory to explain why the link between inequality and saving is negative in OECD countries but positive in emerging Asia. We also offer an econometric analysis of differences in inequality‐saving links between those economies. We find that aggressive financial services lead to a negative link by creating income illusion for overconsumption, but imperfect financial markets contribute to a positive link by interacting with industrial policies as part of growth strategies while ignoring liquidity constraints on consumption.
Maternal alcohol consumption in pregnancy enhances arterial stiffness and alters vasodilator function that varies between vascular beds in fetal sheep
Authors: Parkington Helena C. , Kenna Kelly R. , Sozo Foula , Coleman Harold A. , Bocking Alan , Brien James F. , Harding Richard , Walker David W. , Morley Ruth , Tare Marianne 
Published: April 2014

Key points
To date, the effects of maternal alcohol consumption in pregnancy have focused on neurodevelopmental outcomes, with the impact on the arterial system poorly understood.
In this study we investigated the effects of moderate maternal alcohol consumption (∼3 standard drinks per day) in late pregnancy on the ability of arteries in the fetus to relax, and hence deliver blood, and on arterial stiffness in five important organs.
Maternal alcohol consumption in late pregnancy resulted in a marked increase in stiffness in arteries of the heart, kidney, gut, leg muscle and brain in the fetus, and this could slow contraction and relaxation and overall blood delivery.
Coronary artery endothelial vasodilator function was severely blunted as a result of alcohol exposure, while in contrast endothelium‐dependent relaxation in renal and mesenteric arteries was enhanced.
Together, the results of this study provide a warning for pregnant women and their carers that maternal consumption of ∼3 standard drinks per day, levels that do not evoke physical abnormalities or growth restriction, can dramatically alter arterial function in the fetus.
AbstractWhile the impact of alcohol consumption by pregnant women on fetal neurodevelopment has received much attention, the effects on the cardiovascular system are not well understood. We hypothesised that repeated exposure to alcohol (ethanol) in utero would alter fetal arterial reactivity and wall stiffness, key mechanisms leading to cardiovascular disease in adulthood. Ethanol (0.75 g (kg body weight)–1) was infused intravenously into ewes over 1 h daily for 39 days in late pregnancy (days 95–133 of pregnancy, term ∼147 days). Maternal and fetal plasma ethanol concentrations at the end of the hour were ∼115 mg dl−1, and then declined to apparent zero over 8 h. At necropsy (day 134), fetal body weight and fetal brain–body weight ratio were not affected by alcohol infusion. Small arteries (250–300 μm outside diameter) from coronary, renal, mesenteric, femoral (psoas) and cerebral beds were isolated. Endothelium‐dependent vasodilatation sensitivity was reduced 10‐fold in coronary resistance arteries, associated with a reduction in endothelial nitric oxide synthase mRNA (P = 0.008). Conversely, vasodilatation sensitivity was enhanced 10‐fold in mesenteric and renal resistance arteries. Arterial stiffness was markedly increased (P = 0.0001) in all five vascular beds associated with an increase in elastic modulus and, in cerebral vessels, with an increase in collagen Iα mRNA. Thus, we show for the first time that fetal arteries undergo marked and regionally variable adaptations as a consequence of repeated alcohol exposure. These alcohol‐induced vascular effects occurred in the apparent absence of fetal physical abnormalities or fetal growth restriction.
The role of hydrogen sulphide in the control of breathing in hypoxic zebrafish (Danio rerio)
Authors: Porteus Cosima S. , Abdallah Sara J. , Pollack Jacob , Kumai Yusuke , Kwong Raymond W. M. , Yew Hong M. , Milsom William K. , Perry Steve F. 
Published: April 2014

Key points
Hydrogen sulphide (H2S), a gaseous neurotransmitter, is involved in oxygen sensing in glomus cells, which are oxygen‐sensing cells found in the mammalian carotid body.
Neuroepithelial cells (NECs) are oxygen‐sensing cells of fish and are thought to be phylogenetic precursors of mammalian glomus cells; however, the oxygen‐sensing mechanisms of these cells remain largely unknown.
Both adult and larval zebrafish responded to exogenous H2S by increasing ventilation in a dose‐dependent manner; H2S increased intracellular [Ca2+] in NECs.
Inhibiting endogenous H2S production decreased or abolished the ventilatory response to hypoxia in both adult and larval zebrafish.
The results demonstrate an important role for H2S in oxygen sensing in zebrafish.
AbstractThe current study investigated the role of hydrogen sulphide (H2S) in oxygen sensing, intracellular signalling and promotion of ventilatory responses to hypoxia in adult and larval zebrafish (Danio rerio). Both larval and adult zebrafish exhibited a dose‐dependent increase in ventilation to sodium sulphide (Na2S), an H2S donor. In vertebrates, cystathionine β‐synthase (CBS) and cystathionine γ‐lyase (CSE) are enzymes that catalyse the endogenous production of H2S. In adult zebrafish, inhibition of both CBS and CSE with aminooxyacetate (AOA) and propargyl glycine (PPG) blunted or abolished the hypoxic hyperventilation, and the addition of Na2S to the water partially rescued the effects of inhibiting endogenous H2S production. In zebrafish larvae (4 days post‐fertilization), gene knockdown of either CBS or CSE using morpholinos attenuated the hypoxic ventilatory response. Furthermore, the intracellular calcium concentration of isolated neuroepithelial cells (NECs), which are putative oxygen chemoreceptors, increased significantly when these cells were exposed to 50 μm Na2S, supporting a role for H2S in Ca2+‐evoked neurotransmitter release in these cells. Finally, immunohistochemical labelling showed that NECs dissociated from adult gill contained CBS and CSE, whereas cutaneous NECs in larval zebrafish expressed only CSE. Taken together, these data show that H2S can be produced in the putative oxygen‐sensing cells of zebrafish, the NECs, in which it appears to play a pivotal role in promoting the hypoxic ventilatory response.
Autonomic neural control of heart rate during dynamic exercise: revisited
Authors: White Daniel W. , Raven Peter B. 
Published: April 2014

AbstractThe accepted model of autonomic control of heart rate (HR) during dynamic exercise indicates that the initial increase is entirely attributable to the withdrawal of parasympathetic nervous system (PSNS) activity and that subsequent increases in HR are entirely attributable to increases in cardiac sympathetic activity. In the present review, we sought to re‐evaluate the model of autonomic neural control of HR in humans during progressive increases in dynamic exercise workload. We analysed data from both new and previously published studies involving baroreflex stimulation and pharmacological blockade of the autonomic nervous system. Results indicate that the PSNS remains functionally active throughout exercise and that increases in HR from rest to maximal exercise result from an increasing workload‐related transition from a 4 : 1 vagal–sympathetic balance to a 4 : 1 sympatho–vagal balance. Furthermore, the beat‐to‐beat autonomic reflex control of HR was found to be dependent on the ability of the PSNS to modulate the HR as it was progressively restrained by increasing workload‐related sympathetic nerve activity. In conclusion: (i) increases in exercise workload‐related HR are not caused by a total withdrawal of the PSNS followed by an increase in sympathetic tone; (ii) reciprocal antagonism is key to the transition from vagal to sympathetic dominance, and (iii) resetting of the arterial baroreflex causes immediate exercise‐onset reflexive increases in HR, which are parasympathetically mediated, followed by slower increases in sympathetic tone as workloads are increased.