bluuebunny/crossref_metadata_2025_split huggingface dataset:
Survival and colonization of nematodes in a composting process
Authors: Steel Hanne , Verdoodt Freija , Čerevková Andrea , Couvreur Marjolein , Fonderie Pamela , Moens Tom , Bert Wim 
Published: May 2013

AbstractNematodes are omnipresent in composts and are active in virtually all stages of the composting process. Major shifts in species composition, life strategies, and feeding behavior occur during the composting process. Due to the heat peak, nematodes can be virtually absent, but several taxa appear immediately when the temperatures drop. These comprise both taxa present before the heat peak and new taxa. However, it is not known how nematodes populate the compost. In this study, we aimed to assess the survival and colonization capacity of nematodes in compost. Our results showed that composting processes inaccessible to insects or not in contact with soil did not significantly influence nematode succession during composting. However, differences between treatments were found for some specific taxa (i.e., for Acrostichus sp., Neodiplogasteridae sp., Nygolaimoides sp., and Rhabditidae sp. 1), illustrating the importance of insects for the dispersal of nematodes to compost. Experiments in the lab with the blue bottle fly as a possible carrier demonstrated actual transport of nematodes isolated from compost by the fly (i.e., Halicephalobus cfr. gingivalis, Diploscapter coronatus, Diplogasteritus sp., Acrostichus sp., and Mesorhabditis sp.). Juveniles and dauer stages of Aphelenchoides sp., Panagrolaimus sp., and rhabditids survived an experimentally induced temperature peak, while members of Tylenchidae did not. In conclusion, our results indicate that the rapidly changing nematode community in compost is the result of both differential survival and colonization capacities.
Differential Effects of the β‐Adrenoceptor Blockers Carvedilol and Metoprolol on SQT1‐ and SQT2‐Mutant Channels
Authors: BODI ILONA , FRANKE GERLIND , PANTULU NAGA DEEPA , WU KEZHONG , PEREZ‐FELIZ STEFANIE , BODE CHRISTOPH , ZEHENDER MANFRED , HAUSEN AXEL ZUR , BRUNNER MICHAEL , ODENING KATJA E. 
Published: May 2013

β‐Blocker Effects on SQTS‐Mutant K+ ChannelsBackgroundN588K‐KCNH2 and V307L‐KCNQ1 mutations lead to a gain‐of‐function of IKr and IKs thus causing short‐QT syndromes (SQT1, SQT2). Combined pharmacotherapies using K+‐channel‐blockers and β‐blockers are effective in SQTS. Since β‐blockers can block IKr and IKs, we aimed at determining carvedilol's and metoprolol's electrophysiological effects on N588K‐KCNH2 and V307L‐KCNQ1 channels.MethodsWild‐type (WT)‐KCNH2, WT‐KCNQ1 and mutant N588K‐KCNH2 and V307L‐KCNQ1 channels were expressed in CHO‐K1 or HEK‐293T cells and IKs and IKr were recorded at baseline and during β‐blocker exposure.ResultsCarvedilol (10 μM) reduced IKs tail in WT‐ and V307L‐KCNQ1 by 36.5 ± 5% and 18.6 ± 9% (P < 0.05). IC50 values were 16.3 μM (WT) and 46.1 μM (V307L), indicating a 2.8‐fold decrease in carvedilol's IKs‐blocking potency in V307L‐KCNQ1. Carvedilol's (1 μM) inhibition of the IKr tail was attenuated in N588K‐KCNH2 (4.5 ± 3% vs 50.3 ± 4%, WT, P < 0.001) with IC50 values of 2.8 μM (WT) and 25.4 μM (N588K). Carvedilol's IKr end‐pulse inhibition, however, was increased in N588K‐KCNH2 (10 μM, 60.7 ± 6% vs 36.5 ± 5%, WT, P < 0.01).Metoprolol (100 μM) reduced IKr end‐pulse by 0.23 ± 3% (WT) and 74.1 ± 7% (N588K, P < 0.05), IKr tail by 32.9 ± 10% (WT) and 68.8 ± 7% (N588K, P < 0.05), and reduced IKs end‐pulse by 18.3 ± 5% (WT) and 57.1 ± 11% (V307L, P < 0.05) and IKs tail by 3.3 ± 1% (WT) and 45.1 ± 13 % (V307L, P < 0.05), indicating an increased sensitivity to metoprolol in SQT mutated channels.ConclusionsN588K‐KCNH2 and V307L‐KCNQ1 mutations decrease carvedilol's inhibition of the IKs or IKr tail but increase carvedilol's IKr end‐pulse inhibition and metoprolol's inhibition of tail and end‐pulse currents. These different effects on SQT1 and SQT2 mutated channels should be considered when using β‐blocker therapy in SQTS patients.
Poor reporting quality of key Randomization and Allocation Concealment details is still prevalent among published RCTs in 2011: a review
Authors: Clark Laura , Schmidt Ulrike , Tharmanathan Puvan , Adamson Joy , Hewitt Catherine , Torgerson David 
Published: May 2013

AbstractRationale, aims and objectivesRandomized controlled trials (RCTs) are powerful tools; it is essential that these trials are not only conducted rigorously, but reported accurately. The aim of this paper was to describe the reporting quality among a set of RCTs published in 2011 on methodological details essential to judging the adequacy of allocation concealment methods employed.MethodsMedline was searched using the Ovid platform to identify all those RCTs published in January 2011 in core clinical journals.Methodological details in relation to allocation concealment were extracted from the identified RCTs to allow the reporting quality to be assessed. If the information was not available in the paper the corresponding author was contacted.ResultsEighty‐five papers were identified, 74% (n = 63) endorsed the CONSORT statement. 73% (n = 62) required the author to be contacted for further information. Sequence generation methods were ascertained in 74% of trials, allocation concealment method in 41%, details of who recruited participants and who generated the randomization sequence in 38%.ConclusionsThere is evidence to suggest that in 2011 key methodological information relating to allocation concealment is still not reported well in RCTs. Authors and journal editors need to ensure explicit and clear methods are reported in RCTs published.
A naïve approach for deriving scoring systems to support clinical decision making
Authors: Barbini Paolo , Cevenini Gabriele , Furini Simone , Barbini Emanuela 
Published: May 2013

AbstractRationale, aims and objectivesScoring systems are frequently proposed in medicine to summarize a set of qualitative and quantitative items by means of a numeric score. Their design often requires modelling ability and subjective judgments. This can make it difficult to adapt a scoring system to a clinical setting different from that in which the system was developed. The objective of this study was to discuss an approach to derive scoring systems, which can be easily modified and matched to any scenario.MethodsA naïve Bayes approach was used to develop a scoring system that is completely defined by descriptive tables obtained by frequency counts from the training set. The approach was implemented to build a locally customized scoring system for planning transfusion requirements after cardiac surgery. The performance of this system was evaluated and compared with that of a logistic regression model designed using the same predictors. The working sample was a set of 3182 consecutive patients undergoing cardiac surgery at the University Hospital of Siena, Italy.ResultsThe area under the receiver operating characteristic curve was equal to 0.811 and 0.824 for the scoring system and for the logistic regression model, respectively. This result proves that this global index of discrimination capacity was virtually identical and very good for both models. The values of sensitivity, specificity and overall correct‐classification percentage obtained by the leave‐one‐out method were practically the same for the two models (73.9% versus 75.3%).ConclusionsAn easy‐fitting and trustworthy scoring system can be directly developed using a naïve Bayes approach. The simplicity of its design allows the system to be customized to any specific institution and updated regularly. This aspect has important practical implications because it can encourage the use of scoring systems among clinicians, enabling their performance to be properly assessed in a wider clinical context.
Do clinical and behavioural correlates of obese patients seeking bariatric surgery differ from those of individuals involved in conservative weight loss programme?
Authors: Gradaschi R. , Noli G. , Cornicelli M. , Camerini G. , Scopinaro N. , Adami G. F. 
Published: May 2013

AbstractBackgroundClinical practice has suggested that, in severely obese patients seeking bariatric surgery, clinical conditions, behavioural characteristics and psychological status might all differ from those of their counterparts starting conventional conservative therapy.MethodsTwo groups of obese patients with closely similar body mass values were considered. The first group included individuals voluntarily and spontaneously seeking biliopancreatic diversion and the second group comprised patients at the beginning of a weight loss programme. After anthropometric and metabolic evaluation, the patients underwent an alimentary interview; eating behaviour and psychological status were assessed by Three Factor Eating Questionnaire and by Toronto Alexithymia Scale (TAS).ResultsAmong bariatric candidates, a greater number of individuals with type 2 diabetes and dyslipidaemia and high tendency to disinhibition and susceptibility to hunger scores was observed, whereas the other aspects of eating pattern were essentially similar. In the two groups, no difference in TAS score and or number of patients with alexithymic traits was observed. Finally, a logistic regression model showed that only age and metabolic derangement predicted the bariatric option, whereas eating behaviour or psychological status did not influence individual therapeutic choice.ConclusionsIndependently of the degree of obesity, bariatric surgery was requested by the more metabolically deranged patients, whereas, in the surgical candidates, the eating pattern and psychological conditions were very similar to those of obese persons at the beginning of a conservative weight loss programme. These results suggest a highly realistic and practical attitude in severely obese patients towards obesity and bariatric surgery.
GS6, A Member of the GRAS Gene Family, Negatively Regulates Grain Size in Rice
Authors: Sun Lianjun , Li Xiaojiao , Fu Yongcai , Zhu Zuofeng , Tan Lubin , Liu Fengxia , Sun Xianyou , Sun Xuewen , Sun Chuanqing 
Published: May 2013

AbstractGrain size is an important yield‐related trait in rice. Intensive artificial selection for grain size during domestication is evidenced by the larger grains of most of today's cultivars compared with their wild relatives. However, the molecular genetic control of rice grain size is still not well characterized. Here, we report the identification and cloning of Grain Size 6 (GS6), which plays an important role in reducing grain size in rice. A premature stop at the +348 position in the coding sequence (CDS) of GS6 increased grain width and weight significantly. Alignment of the CDS regions of GS6 in 90 rice materials revealed three GS6 alleles. Most japonica varieties (95%) harbor the Type I haplotype, and 62.9% of indica varieties harbor the Type II haplotype. Association analysis revealed that the Type I haplotype tends to increase the width and weight of grains more than either of the Type II or Type III haplotypes. Further investigation of genetic diversity and the evolutionary mechanisms of GS6 showed that the GS6 gene was strongly selected in japonica cultivars. In addition, a “ggc” repeat region identified in the region that encodes the GRAS domain of GS6 played an important historic role in the domestication of grain size in rice. Knowledge of the function of GS6 might aid efforts to elucidate the molecular mechanisms that control grain development and evolution in rice plants, and could facilitate the genetic improvement of rice yield.
Involvement of α2‐antiplasmin in dendritic growth of hippocampal neurons
Authors: Kawashita Eri , Kanno Yosuke , Asayama Haruka , Okada Kiyotaka , Ueshima Shigeru , Matsuo Osamu , Matsuno Hiroyuki 
Published: May 2013

AbstractThe α2‐Antiplasmin (α2AP) protein is known as a principal physiological inhibitor of plasmin, but we previously demonstrated that it acts as a regulatory factor for cellular functions independent of plasmin. α2AP is highly expressed in the hippocampus, suggesting a potential role for α2AP in hippocampal neuronal functions. However, the role for α2AP was unclear. This study is the first to investigate the involvement of α2AP in the dendritic growth of hippocampal neurons. The expression of microtubule‐associated protein 2, which contributes to neurite initiation and neuronal growth, was lower in the neurons from α2AP−/− mice than in the neurons from α2AP+/+ mice. Exogenous treatment with α2AP enhanced the microtubule‐associated protein 2 expression, dendritic growth and filopodia formation in the neurons. This study also elucidated the mechanism underlying the α2AP‐induced dendritic growth. Aprotinin, another plasmin inhibitor, had little effect on the dendritic growth of neurons, and α2AP induced its expression in the neurons from plaminogen−/− mice. The activation of p38 MAPK was involved in the α2AP‐induced dendritic growth. Therefore, our findings suggest that α2AP induces dendritic growth in hippocampal neurons through p38 MAPK activation, independent of plasmin, providing new insights into the role of α2AP in the CNS.
Distinct intrinsic and synaptic properties of pre‐sympathetic and pre‐parasympathetic output neurons in Barrington's nucleus
Authors: Guo Yue‐Xian , Li De‐Pei , Chen Shao‐Rui , Pan Hui‐Lin 
Published: May 2013

AbstractBarrington's nucleus (BN), commonly known as the pontine micturition center, controls micturition and other visceral functions through projections to the spinal cord. In this study, we developed a rat brain slice preparation to determine the intrinsic and synaptic mechanisms regulating pre‐sympathetic output (PSO) and pre‐parasympathetic output (PPO) neurons in the BN using patch‐clamp recordings. The PSO and PPO neurons were retrogradely labeled by injecting fluorescent tracers into the intermediolateral region of the spinal cord at T13‐L1 and S1‐S2 levels, respectively. There were significantly more PPO than PSO neurons within the BN. The basal activity and membrane potential were significantly lower in PPO than in PSO neurons, and A‐type K+ currents were significantly larger in PPO than in PSO neurons. Blocking A‐type K+ channels increased the excitability more in PPO than in PSO neurons. Stimulting μ‐opioid receptors inhibited firing in both PPO and PSO neurons. The glutamatergic EPSC frequency was much lower, whereas the glycinergic IPSC frequency was much higher, in PPO than in PSO neurons. Although blocking GABAA receptors increased the excitability of both PSO and PPO neurons, blocking glycine receptors increased the firing activity of PPO neurons only. Furthermore, blocking ionotropic glutamate receptors decreased the excitability of PSO neurons but paradoxically increased the firing activity of PPO neurons by reducing glycinergic input. Our findings indicate that the membrane and synaptic properties of PSO and PPO neurons in the BN are distinctly different. This information improves our understanding of the neural circuitry and central mechanisms regulating the bladder and other visceral organs.
Diethylmaleate and iodoacetate in combination caused profound cell death in astrocytes
Authors: Liao Su‐Lan , Ou Yen‐Chuan , Chang Cheng‐Yi , Chen Wen‐Ying , Kuan Yu‐Hsiang , Wang Wen‐Yi , Pan Hung‐Chuan , Chen Chun‐Jung 
Published: May 2013

AbstractEnergy failure and oxidative stress have been implicated in the pathogenesis of ischemia. Here, we report a potential link between cytosolic phospholipase A2 (cPLA2) activation and energy failure/oxidative stress‐induced astrocyte damage involving reactive oxygen species (ROS), protein kinase C‐α (PKC‐α), Src, Raf, and extracellular signal‐regulated kinase (ERK) signaling and concurrent elevation of endogenous chelatable zinc. Energy failure and oxidative stress were produced by treating astrocytes with glycolytic inhibitor iodoacetate and glutathione chelator diethylmaleate, respectively. Diethylmaleate and iodoacetate in combination caused augmented damage to astrocytes in a time‐ and concentration‐dependent manner. The cell death caused by diethylmaleate/iodoacetate was accompanied by increased ROS generation, PKC‐α membrane translocation, Src, Raf, ERK, and cPLA2 phosphorylation. Pharmacological studies revealed that these activations all contributed to diethylmaleate/iodoacetate‐induced astrocyte death. Intriguingly, the mobilization of endogenous chelatable zinc was observed in diethylmaleate/iodoacetate‐treated astrocytes. Zinc appears to act as a downstream mediator in response to diethylmaleate/iodoacetate treatment because of the attenuating effects of its chelator N,N,N′,N′‐tetrakis(2‐pyridylmethyl)ethylenediamine. These observations indicate that ROS/PKC‐α, Src/Raf/ERK signaling and cPLA2 are active participants in diethylmaleate/iodoacetate‐induced astrocyte death and contribute to a vicious cycle between the depletion of ATP/glutathione and the mobilization of chelatable zinc as critical upstream effectors in initiating cytotoxic cascades.
imageEnergy failure and oxidative stress have been implicated in the pathogenesis of ischemia and cell death. Through the application of the glycolytic inhibitor iodoacetate and the glutathione chelator diethylmaleate, we report a potential link between cytosolic phospholipase A2 (cPLA2) activation and energy failure/oxidative stress‐induced astrocyte damage involving reactive oxygen species (ROS), signaling through the kinases PKC‐α, Src, Raf, and ERK and concurrent elevation of endogenous chelatable zinc.
Evolutionary conservation of an atypical glucocorticoid‐responsive element in the human tyrosine hydroxylase gene
Authors: Sheela Rani C. S. , Soto‐Pina Alexandra , Iacovitti Lorraine , Strong Randy 
Published: May 2013

AbstractThe human tyrosine hydroxylase (hTH) gene has a 42 bp evolutionarily conserved region designated (CR) II at −7.24 kb, which bears 93% homology to the region we earlier identified as containing the glucocorticoid response element, a 7 bp activator protein‐1 (AP‐1)‐like motif in the rat TH gene. We cloned this hTH‐CRII region upstream of minimal basal hTH promoter in luciferase (Luc) reporter vector, and tested glucocorticoid responsiveness in human cell lines. Dexamethasone (Dex) stimulated Luc activity of hTH‐CRII in HeLa cells, while mifepristone, a glucocorticoid receptor (GR) antagonist, prevented Dex stimulation. Deletion of the 7 bp 5′‐TGACTAA at −7243 bp completely abolished the Dex‐stimulated Luc activity of hTH‐CRII construct. The AP‐1 agonist, tetradeconoyl‐12,13‐phorbol acetate (TPA), also stimulated hTH promoter activity, and Dex and TPA together further accentuated this response. Chromatin immunoprecipitation assays revealed the presence of both GR and AP‐1 proteins, especially Jun family members, at this hTH promoter site. Dex did not stimulate hTH promoter activity in a catecholaminergic cell line, which had low endogenous GR levels, but did activate the response when GR was expressed exogenously. Thus, our studies have clearly identified a glucocorticoid‐responsive element in a 7 bp AP‐1‐like motif in the promoter region at −7.24 kb of the human TH gene.
Human choroid plexus papilloma cells efficiently transport glucose and vitamin C
Authors: Ulloa Viviana , García‐Robles María , Martínez Fernando , Salazar Katterine , Reinicke Karin , Pérez Fernando , Godoy David F. , Godoy Alejandro S. , Nualart Francisco 
Published: May 2013

AbstractIn vitro and in vivo studies suggest that the basolateral membrane of choroid plexus cells, which is in contact with blood vessels, is involved in the uptake of the reduced form of vitamin C, ascorbic acid (AA), through the sodium‐vitamin C cotransporter, (SVCT2). Moreover, very low levels of vitamin C were observed in the brains of SVCT2‐null mice. The oxidized form of vitamin C, dehydroascorbic acid (DHA), is incorporated through the facilitative glucose transporters (GLUTs). In this study, the contribution of SVCT2 and GLUT1 to vitamin C uptake in human choroid plexus papilloma (HCPP) cells in culture was examined. Both the functional activity and the kinetic parameters of GLUT1 and SVCT2 in cells isolated from HCPP were observed. Finally, DHA uptake by GLUT1 in choroid plexus cells was assessed in the presence of phorbol‐12‐myristate‐13‐acetate (PMA)‐activated human neutrophils. A marked increase in vitamin C uptake by choroid plexus cells was observed that was associated with superoxide generation and vitamin C oxidation (bystander effect). Thus, vitamin C can be incorporated by epithelial choroid plexus papilloma cells using the basolateral polarization of SVCT2 and GLUT1. This mechanism may be amplified with neutrophil infiltration (inflammation) of choroid plexus tumors.imageIn choroid plexus papilloma cells, the vitamin C transporters SVCT2 and GLUT1 are polarized to the basolateral epithelial membrane, where SVCT2 is essential for AA flux from the blood vessels into the brain. However, neutrophils, attracted by inflammation or the tumor microenvironment, can oxidize extracellular AA to DHA, thereby enabling its uptake through GLUT1. For the first time, we show the in vivo and in vitro basolateral co‐distribution of functional SVCT2 and GLUT1 in epithelial cells. We postulate that patients with choroid plexus papillomas may continue to transport vitamin C from the blood to CSF. However, increased transport of oxidized vitamin C could generate pro‐oxidative conditions that may help control tumor growth.
Voiding Dysfunction in Spinocerebellar Ataxia Type 31
Authors: SUGIYAMA Megumi , SAKAKIBARA Ryuji , TATENO Fuyuki , YANO Masashi , TAKAHASHI Osamu , KISHI Masahiko , TSUYUSAKI Yohei , YAMAMOTO Tatsuya , UCHIYAMA Tomoyuki , YAMANISHI Tomonori , YAMAGUCHI Chiharu , NOMURA Fumio 
Published: May 2013

ObjectiveTo describe a case of SCA31 who presented with possible neurogenic voiding dysfunction.MethodsA case report.ResultsA 73‐year‐old man with a 5‐year history of cerebellar ataxia developed partial urinary retention. His father and a sister had cerebellar ataxia. Brain magnetic resonance imaging revealed cerebellar atrophy, and gene analysis revealed TGGAA repeat prolongation, and he was diagnosed with spinocerebellar ataxia 31. Urodynamics revealed normal bladder filling but a slightly weak detrusor and a post‐void residual urine volume of 130 mL, whereas his prostate volume was normal (26 mL). External sphincter electromyography revealed neurogenic change in the motor unit potentials. In order to lessen the post‐void residual, hewas started on 15mg/day pilocarpine with benefit. The weak detrusor and sphincter electromyography abnormality indicated involvement of the sacral spinal cord in this disorder.ConclusionNeurogenic urinary retention in SCA31 can be listed in the clinical differential diagnosis of cerebellar ataxia. However, possible outflow obstruction in men should always be explored.