bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pneumonia and the incidence of cancer: a Danish nationwide cohort study
Authors: Søgaard K. K. , Farkas D. K. , Pedersen L. , Weiss N. S. , Thomsen R. W. , Sørensen H.T. 
Published: May 2014

AbstractObjectivesTo examine the risk of a subsequent pulmonary or extra‐pulmonary cancer diagnosis following a first‐time hospital‐based diagnosis of pneumonia.DesignPopulation‐based cohort study using Danish medical registries.SettingAll hospitals in Denmark.SubjectsA total of 342 609 patients with a first‐time hospital‐based (inpatient, emergency room or outpatient clinic) diagnosis of pneumonia between 1995 and 2011.Main outcome measuresWe quantified the excess risk of various cancers amongst pneumonia patients compared to the expected risk in the general population, using relative [standardised incidence ratios (SIRs)] and absolute risk calculations. Follow‐up started 1 month after a hospital‐based diagnosis of pneumonia and ended on 31 December 2011.ResultsA total of 28 496 cancers were observed, compared with 21 625 expected, amongst 342 609 pneumonia patients followed for a median of 4.2 years. The absolute risk of a cancer diagnosis 1 to <6 months following a pneumonia diagnosis was 1.4%, with a corresponding SIR of 2.48 [95% confidence interval (CI) 2.41–2.55]. This was mainly due to an increased risk of lung cancer (eightfold) and haematological cancers (fourfold). The SIR for any cancer remained increased at 1.35 (95% CI 1.30–1.40) during 6–12 months of follow‐up, and 1.20 (95% CI 1.18–1.22) during 1–5 years of follow‐up. Beyond 5 years, an increased risk was maintained for lung, oesophageal, liver and bladder cancers, squamous cell carcinoma of the skin, lymphoma and multiple myeloma.ConclusionsA hospital‐based pneumonia diagnosis was associated with an increased risk of a cancer diagnosis, especially in the ensuing months, but the absolute risk was small.
Evidence of Cotton leaf curl Burewala virus Variant and its Associate Betasatellite Causing Yellow Mosaic of Eggplant (Solanum melongena) in Pakistan
Authors: Ullah Rahim , Akhtar Khalid P. , Hassan Ishtiaq , Saeed Muhammad , Sarwar Nighat , Mansoor Shahid 
Published: May 2014

AbstractEggplant (Solanum melongena L.) plants with severe leaf mosaic and mottling were found in a kitchen garden near cotton fields in Pakistan. Rolling Circle Amplification products from six of the naturally infected eggplant plants, subjected to PCR, successfully amplified expected products of 2.8 and 1.4 kb using begomovirus and betasatellite‐specific primers, respectively. Based on 99% nucleotide sequence identity, the virus was identified as a variant of Cotton leaf curl Burewala virus (CLCuBuV) (GenBank Accession No. HG428709). Likewise, the sequenced betasatellite with a maximum of 97% nucleotide sequence identity was recognized as a new variant of Cotton leaf curl Multan betasatellite (CLCuMuBMul) (GenBank Accession No. HG428708). The symptomatic induction of Cotton leaf curl disease in CLCuBuV susceptible cotton genotype CIM‐496 by back‐indexing further confirmed the presence of CLCuBuV in eggplant. This is the first report of CLCuBuV and its associate betasatellite in naturally infected plants of eggplant.
Identification and Characterization of the Causal Agent of Gummy Stem Blight from Muskmelon and Watermelon in East China
Authors: Li Ping‐Fang , Ren Run‐Sheng , Yao Xie‐Feng , Xu Jin‐Hua , Babu Binoy , Paret Mathews L. , Yang Xing‐Ping 
Published: May 2014

AbstractGummy stem blight (GSB) is one of the most destructive foliar diseases of cucurbits, worldwide. To identify and characterize the pathogen which causes GSB on watermelon and muskmelon in East China, morphological characteristics, pathogenicity assays as well as sequence characterization of the rDNA internal transcribed spacer (ITS) were performed on 41 isolates collected from Jiangsu, Zhejiang, Anhui and Jiangxi provinces. The mycelia of all the isolates were white on top and olivaceous green to black with concentric circles at the bottom on potato‐dextrose agar medium. The isolates differed significantly on aggressiveness based on pathogenicity assays. rDNA‐ITS sequences and phylogenetic analysis confirmed the isolates as Didymella bryoniae. The isolates were found to be highly identical with the exception of 13 isolates, which had a guanine substitution instead of adenine at position 131 of the ITS.
Medical Hypothesis: Loss of the Endocrine Function of the Prostate Is Important to the Pathophysiology of Postprostatectomy Erectile Dysfunction
Authors: Kacker Ravi , Morgentaler Abraham , Traish Abdulmaged 
Published: May 2014

Abstract

Introduction
Three decades after the first nerve-sparing radical prostatectomy, postoperative erectile dysfunction (ED) remains a challenging and common problem. Despite considerable advances and improvements in surgical techniques, full recovery of erectile function remains elusive even for young, potent men. This suggests, ipso facto, that factors other than surgical technique must be important to recovery of erectile function.

Aim
This study aims to review evidence that the prostate is an endocrine gland with contributions to local and systemic concentrations of 5α-dihydrotestosterone (5α-DHT), a potent androgen shown to be critical to penile physiology.

Methods
Literature review of human and animal studies related to endocrine role of prostate and postoperative recovery of erectile function.

Main Outcome Measures
Effect of 5α-DHT on erectile function and recovery after surgical injury.

Results
We advance the following hypothesis: “Loss of endocrine function of the prostate, specifically reduced local 5α-DHT concentration plays a major role in the failure of full recovery of erectile function following anatomic nerve-sparing radical prostatectomy.”

Conclusions
We propose two separate, yet interrelated, mechanisms whereby the loss of 5α-DHT interferes with postoperative recovery of erectile function: (i) 5α-DHT contributes to cavernous nerve integrity and its ability to recover from surgical insult. (ii) 5α-DHT is important to the structural/functional integrity of penile tissues and erectile physiology.
Human microRNA hsa‐miR‐1231 suppresses hepatitis B virus replication by targeting core mRNA
Authors: Kohno T. , Tsuge M. , Murakami E. , Hiraga N. , Abe H. , Miki D. , Imamura M. , Ochi H. , Hayes C. N. , Chayama K. 
Published: May 2014

SummaryPathogen‐specific miRNA profiles might reveal potential new avenues for therapy. To identify miRNAs directly associated with hepatitis B virus (HBV) in hepatocytes, we performed a miRNA array analysis using urokinase‐type plasminogen activator (uPA)–severe combined immunodeficiency (SCID) mice where the livers were highly repopulated with human hepatocytes and human immune cells are absent. Mice were inoculated with HBV‐infected patient serum samples. Eight weeks after HBV infection, human hepatocytes were collected from liver tissues, and miRNAs were analysed using the Toray 3D array system. The effect of miRNAs on HBV replication was analysed using HBV‐transfected HepG2 cells. Four miRNAs, hsa‐miR‐486‐3p, hsa‐miR‐1908, hsa‐miR‐675 and hsa‐miR‐1231 were upregulated in mouse and human livers with HBV infection. These miRNAs were associated with immune response pathways such as inflammation mediated by chemokine and cytokine signalling. Of these miRNAs, hsa‐miR‐1231, which showed high homology with HBV core and HBx sequences, was most highly upregulated. In HBV‐transfected HepG2 cells, overexpression of hsa‐miR‐1231 resulted in suppression of HBV replication with HBV core reduction. In conclusion, a novel interaction between hsa‐miR‐1231 and HBV replication was identified. This interaction might be useful in developing new therapeutic strategies against HBV.
Radioembolization of hepatocellular carcinoma activates liver regeneration, induces inflammation and endothelial stress and activates coagulation
Authors: Fernandez‐Ros Nerea , Iñarrairaegui Mercedes , Paramo Jose A. , Berasain Carmen , Avila Matias A. , Chopitea Ana , Varo Nerea , Sarobe Pablo , Bilbao Jose I. , Dominguez Ines , D'Avola Delia , Herrero J. Ignacio , Quiroga Jorge , Sangro Bruno 
Published: May 2014

AbstractBackground & AimsRadioembolization may rarely induce liver disease resulting in a syndrome that is similar to veno‐occlusive disease complicating bone marrow transplantation where inflammation, endothelial cell activation and thrombosis are likely involved. We hypothesized that similar mechanisms could be implicated in radioembolization‐induced liver disease (REILD). Moreover, lobar radioembolization may induce hypertrophy of the non‐treated hemiliver most probably by inducing liver regeneration.MethodsIn patients with hepatocellular carcinoma, we prospectively studied serum levels of markers of liver regeneration, oxidative stress, pro‐inflammatory pathways, endothelial activation and coagulation parameters over 2 months after radioembolization.ResultsAlthough REILD did not occur among 14 treated patients, a decrease in effective liver blood flow was observed. Radioembolization was followed by a persistent increase in pro‐inflammatory (interleukin 6 and 8) and oxidative stress (malondyaldehide) markers, an induction of endothelial injury markers (vW factor and PAI‐1) and an activation of the coagulation cascade (factor VIII, PAI‐1, D‐Dimer) as well as a significant increase in factors related to liver regeneration (FGF‐19 and HGF).ConclusionRadioembolization activates liver regeneration, produces oxidative stress, activates inflammatory cytokines and induces endothelial injury with partial activation of the coagulation cascade. These findings may have implications in the pathogenesis, prevention and therapy of REILD and in the development of new therapies to enhance hypertrophy with a surgical perspective.
Artificial Marine Micro‐Reserves Networks (AMMRNs): an innovative approach to conserve marine littoral biodiversity and protect endangered species
Authors: García‐Gómez José C. , Guerra‐García José M. , Espinosa Free , Maestre Manuel J. , Rivera‐Ingraham Georgina , Fa Darren , González Alexander R. , Ruiz‐Tabares Aurora , López‐Fé Carlos M. 
Published: May 2014

AbstractCoastal engineering works, especially the outer breakwaters of ports where environmental conditions are usually good, often constitute new habitats for marine littoral species. Their potential indirect contribution to the regeneration and conservation of protected species opens up a new perspective in protection of marine biodiversity. This is particularly true when these works harbour, as we show here, important reproductive populations of species that are threatened or even in danger of extinction. We provide integrated data on protected marine species in Southern Iberia established on different substrata (quarried dolomitic rocks, concrete cubic blocks, concrete tetrapods and vertical concrete walls) that are used in the construction of artificial levees that could potentially be Artificial Marine Micro‐Reserves (AMMRs). We also present the first evidence of the ‘reserve effect’ in potential AMMRs and we discuss the need for the creation of AMMRs including their effective networking (AMMRNs), supporting data for which has been observed by studying coastal facilities subjected to strict access restrictions (for security reasons, not conservation). These facilities have acted as valuable proxies and, in reality, potentially act as AMMRs, as well as having a role in helping to detect and control invasive species. We discuss the ecological engineering aspects related to the design and type of materials used in coastal constructions with a view to aiding the integration of these into existing coastal ecosystems as well as promoting greater settlement of species and therefore increases in biodiversity. Finally, the environmental implications of AMMRNs within the future implementation strategy of the Water Framework Directive 2000/60 EC are also discussed.
Temporal variation in cannibalistic infanticide by the shore crab Hemigrapsus oregonensis: implications for reproductive success
Authors: Miller Seth H. , Morgan Steven G. 
Published: May 2014

AbstractLarvae of benthic marine organisms are released amid high densities of suspension feeding and predatory adults and are highly subject to being consumed, even by conspecifics or their own parent. During laboratory feeding trials conducted in June 2006, female shore crabs (Hemigrapsus oregonensis) from Stege Marsh in San Francisco Bay (37°54.530′ N, 122°19.734′ W) that released their larvae during the previous 24 h ate fewer conspecific larvae than females that had not recently released larvae, though the behavior was not repeated during similar trials in 2007. Additionally, the number of larvae eaten increased with increasing starvation time, and hungrier females showed a trend toward eating more larvae from a different species (Carcinus maenas) than larvae of conspecifics. Thus, suppression of suspension feeding may reduce conspecific predation of newly released larvae, but this response partially depends on hunger level. This is the first time crabs have been shown to suppress feeding to reduce cannibalism of larvae, and this behavior could affect reproductive success and population dynamics.
Generation of a ToxA knockout strain of the wheat tan spot pathogen Pyrenophora tritici‐repentis
Authors: Moffat Caroline S. , See Pao Theen , Oliver Richard P. 
Published: May 2014

SummaryThe necrotrophic fungal pathogen Pyrenophora tritici‐repentis causes tan spot, a major disease of wheat, throughout the world. The proteinaceous effector ToxA is responsible for foliar necrosis on ToxA‐sensitive wheat genotypes. The single copy ToxA gene was deleted from a wild‐type race 1 P. tritici‐repentis isolate via homologous recombination of a knockout construct. Expression of the ToxA transcript was found to be absent in transformants (toxa), as was ToxA protein production in fungal culture filtrates. Plant bioassays were conducted to test transformant pathogenicity. The toxa strains were unable to induce necrosis on ToxA‐sensitive wheat genotypes. To our knowledge, this is the first demonstration of a targeted gene knockout in P. tritici‐repentis. The ability to undertake gene deletions will facilitate the characterization of other pathogenicity effectors of this economically significant necrotroph.
A transcription factor FgSte12 is required for pathogenicity in Fusarium graminearum
Authors: Gu Qin , Zhang Chengqi , Liu Xin , Ma Zhonghua 
Published: May 2014

SummaryA conserved mitogen‐activated protein kinase (MAPK) cascade homologous to the yeast Fus3/Kss1 mating/filamentation pathway is involved in the regulation of vegetative development and pathogenicity in Fusarium graminearum. However, little is known about the downstream transcription factors of this pathway. In Saccharomyces cerevisiae, the homeodomain protein Ste12 is a key transcription factor activated by Fus3/Kss1. In this study, we characterized a Ste12 orthologue FgSte12 in F. graminearum. The FgSTE12 deletion mutant (ΔFgSte12) was impaired in virulence and in the secretion of cellulase and protease, although it did not show recognizable phenotype changes in hyphal growth, conidiation or deoxynivalenol (DON) biosynthesis. In addition, ΔFgSte12 and the FgGPMK1 (a FUS3/KSS1‐related MAPK gene) mutant shared several phenotypic traits. Furthermore, we found that FgGpmk1 controls the nuclear localization of FgSte12. Yeast two‐hybrid and affinity capture assays indicated that FgSte12 interacts with the FgSte11–Ste7–Gpmk1 complex. Taken together, these results indicate that FgSte12 is a downstream target of FgSte11–Ste7–Gpmk1 and plays an important role in pathogenicity in F. graminearum.
TRPM8 has a key role in experimental colitis‐induced visceral hyperalgesia in mice
Authors: Hosoya T. , Matsumoto K. , Tashima K. , Nakamura H. , Fujino H. , Murayama T. , Horie S. 
Published: May 2014

AbstractBackgroundTransient receptor potential channel melastatin 8 (TRPM8) is activated by cold temperatures and cooling agents (menthol and icilin). Recent studies showed TRPM8 is expressed in visceral organs and peripheral sensory pathways. However, the role of TRPM8 in visceral hyperalgesia is poorly understood in pathological states such as inflammatory bowel disease. Hence, we investigated the distribution of TRPM8 and its involvement in visceral hyperalgesia in experimental colitis mice.MethodsTRPM8 immunoreactivity was detected using immunohistochemical staining with fluorescein‐conjugated tyramide amplification. Visceral hyperalgesia was measured by the intracolonic administration of TRPM8 agonist, WS‐12, in control and dextran sodium sulfate (DSS)‐induced colitis mice.Key ResultsTRPM8 immunoreactivity in the distal colon was much higher than in the transverse and proximal colon under physiological conditions. TRPM8 immunoreactivity markedly increased in the distal colon mucosa of DSS‐induced colitis mice compared with control mice. The number of TRPM8 nerve fibers in mucosa of DSS‐ or 2,4,6‐trinitrobenzene sulfonic acid‐induced colitis model mice drastically increased compared with control mice. TRPM8 immunoreactivities colocalized with the calcitonin gene‐related peptide‐ and substance P‐immunoreactive nerve fibers in the mucosa. Intracolonic administration of WS‐12 induced behavioral visceral pain‐like responses. The numbers of these responses in the colitis model mice were 3 times higher than in control mice, and were decreased by pretreatment with the TRPM8 channel blocker AMTB.Conclusions & InferencesIncreased expression of TRPM8 may contribute to the visceral hyperalgesia of experimental colitis.
Atrial Tachycardias Utilizing the Ligament of Marshall Region Following Single Ring Pulmonary Vein Isolation for Atrial Fibrillation
Authors: CHIK WILLIAM W.B. , CHAN JACKY KIT , ROSS DAVID L. , WAGSTAFF JACKIE , KIZANA EDDY , THIAGALINGAM ARAVINDA , KOVOOR PRAMESH , THOMAS STUART P. 
Published: May 2014

BackgroundOrganized atrial tachycardias (OATs) after pulmonary vein isolation (PVI) procedure are common. Arrhythmia mechanisms include mitral annular, ring gap, or roof‐dependent gap‐related flutters. In this series, we describe a mechanism of arrhythmia utilizing the ridge between left pulmonary vein (PV) and left atrial appendage (LAA) in the Ligament of Marshall (LOM) region.Methods and ResultsFive tachycardias involving the LOM region were identified from a group of 240 patients who underwent a single ring PVI procedure for symptomatic atrial fibrillation. The common characteristics of these tachycardias were the endocardial breakout over a broad area adjacent to the LOM region, presence of presystolic or mid‐diastolic potentials, and abolition by ablation of the presystolic or mid‐diastolic potentials remote from the endocardial breakout site. In all five cases, tachycardias were present after isolation of the veins and posterior left atria. All demonstrated characteristic areas of very slow conduction in the LOM region highlighted by presence of either low voltage, long duration fractionated potentials, or mid‐diastolic potentials with a fixed temporal relationship to the subsequent endocardial activation. The pattern of activation and termination of tachycardia during ablation was consistent with an arrhythmia utilizing an electrically insulated tract within LOM and the PV‐LAA ridge region.ConclusionsWe identified a pattern of arrhythmias involving a concealed presystolic component and a broad endocardial breakout site related to the LOM region. Successful ablation site involved careful identification of small diastolic potentials in the LAA/ridge region or adjacent to the coronary sinus.
Acute Decrease of Cerebral Oxygen Saturation during Rapid Ventricular and Supraventricular Rhythm: A Pilot Study
Authors: WUTZLER ALEXANDER , OTTO NATALIE , GRÄSER SASKIA , BOLDT LEIF‐HENDRIK , HUEMER MARTIN , PARWANI ABDUL , HAVERKAMP WILHELM , STORM CHRISTIAN 
Published: May 2014

BackgroundMonitoring of cerebral tissue oxygen saturation (SctO2) reflects cerebral microcirculation. We sought to characterize the decrease in SctO2 during supraventricular tachycardia (SVT) and ventricular tachycardia (VT) in adults.MethodsTwenty patients (mean age: 46.3 ± 18.1 years, 40% men) were included. Rapid atrial and ventricular pacing (200/min) was used as a model for VT and SVT. Near‐infrared spectroscopy (NIRS) was used to measure SctO2.ResultsAtrial stimulation decreased right (P = 0.014) and left (P = 0.019) hemispheric SctO2 compared to baseline. Ventricular stimulation also decreased right (P < 0.001) and left (P < 0.001) hemispheric SctO2. A negative correlation between age and minimal value under stimulation was found for atrial (right SctO2 r = –0.641, P = 0.034; left SctO2 r = –0.694, P = 0.018) and ventricular pacing (right SctO2 r = –0.564, P = 0.01; left SctO2 r = –0.604, P = 0.005). A positive correlation was found between left ventricular ejection fraction (LVEF) and minimal value under ventricular stimulation (right SctO2 r = 0.567, P = 0.009; left SctO2 r = 0.471, P = 0.036).ConclusionCerebral perfusion decreased during simulated SVT and VT and is influenced by age and LVEF. Clinicians can consider NIRS monitoring in patients during ablation procedures and in critical care. NIRS may especially be appropriate for the elderly and for patients with impaired LVEF.
Left Ventricular Hypertrophy and Antiarrhythmic Drugs in Atrial Fibrillation: Impact on Mortality
Authors: CHUNG ROY , HOUGHTALING PENNY L. , TCHOU MICHAEL , NIEBAUER MARK J. , LINDSAY BRUCE D. , TCHOU PATRICK J. , CHUNG MINA K. 
Published: May 2014

BackgroundDespite sparse clinical data, current atrial fibrillation (AF) guidelines favor amiodarone as a drug of choice for patients with left ventricular hypertrophy (LVH).ObjectiveThis study tested the hypothesis that patients with persistent AF and LVH on nonamiodarone antiarrhythmics have higher mortality compared to patients on amiodarone.MethodsIn an observational cohort analysis of patients who underwent cardioversion for AF, patients with LVH, defined as left ventricular wall thickness ≥1.4 cm, by echocardiogram prior to their first cardioversion, were included; clinical data, including antiarrhythmic drugs and ejection fraction (LVEF), were collected. Mortality, determined via the Social Security Death Index, was analyzed using Kaplan‐Meier and Cox proportional hazards models to determine whether antiarrhythmic drugs were associated with higher mortality.ResultsIn 3,926 patients, echocardiographic wall thickness was available in 1,399 (age 66.8 ± 11.8 years, 67% male, LVEF 46 ± 15%, septum 1.3 ± 0.4, posterior wall 1.2 ± 0.2 cm), and 537 (38%) had LVH ≥1.4 cm. Among 537 patients with LVH, mean age was 67.5 ± 11.7 years, 76.4% were males, and mean LVEF was 48.3 ± 13.3%. Amiodarone was associated with lower survival (log rank P = 0.001), including after adjusting for age, LVEF, and coronary artery disease (P = 0.023). In propensity‐score matched cohorts with LVH treated with no drugs, nonamiodarone antiarrhythmic drugs (non‐AADs), or amiodarone (N = 65 each group), there was early lower survival in patients on amiodarone (P = 0.05).ConclusionsPatients with persistent AF and LVH on non‐AADs do not have higher mortality compared to patients on amiodarone. Importantly, these findings do not support amiodarone as a superior choice in patients with LVH.