bluuebunny/crossref_metadata_2025_split huggingface dataset:
Induction of the inflammatory regulator A20 by gibberellic acid in airway epithelial cells
Authors: Reihill J A , Malcomson B , Bertelsen A , Cheung S , Czerwiec A , Barsden R , Elborn J S , Dürkop H , Hirsch B , Ennis M , Kelly C , Schock B C 
Published: May 2015

Background and PurposeNF‐κB‐driven inflammation is negatively regulated by the zinc finger protein A20. Gibberellic acid (GA3) is a plant‐derived diterpenoid with documented anti‐inflammatory activity, which is reported to induce A20‐like zinc finger proteins in plants. Here, we sought to investigate the anti‐inflammatory effect of GA3 in airway epithelial cells and determine if the anti‐inflammatory action relates to A20 induction.Experimental ApproachPrimary nasal epithelial cells and a human bronchial epithelial cell line (16HBE14o‐) were used. Cells were pre‐incubated with GA3, stimulated with Pseudomonas aeruginosa LPS; IL‐6 and IL‐8 release, A20, NF‐κB and IκBα expression were then evaluated. To determine if any observed anti‐inflammatory effect occurred via an A20‐dependent mechanism, A20 was silenced using siRNA.Key ResultsCells pre‐incubated with GA3 had significantly increased levels of A20 mRNA (4 h) and protein (24 h), resulting in a significant reduction in IL‐6 and IL‐8 release. This effect was mediated via reduced IκBα degradation and reduced NF‐κB (p65) expression. Furthermore, the anti‐inflammatory action of GA3 was abolished in A20‐silenced cells.Conclusions and ImplicationsWe showed that A20 induction by GA3 attenuates inflammation in airway epithelial cells, at least in part through its effect on NF‐κB and IκBα. GA3 or gibberellin‐derived derivatives could potentially be developed into anti‐inflammatory drugs for the treatment of chronic inflammatory diseases associated with A20 dysfunction.Linked ArticlesThis article is part of a themed section on Inflammation: maladies, models, mechanisms and molecules. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2016.173.issue-4
A mathematical model of the evolution of individual differences in developmental plasticity arising through parental bet‐hedging
Authors: Frankenhuis Willem E. , Panchanathan Karthik , Belsky Jay 
Published: May 2015

AbstractChildren vary in the extent to which their development is shaped by particular experiences (e.g. maltreatment, social support). This variation raises a question: Is there no single level of plasticity that maximizes biological fitness? One influential hypothesis states that when different levels of plasticity are optimal in different environmental states and the environment fluctuates unpredictably, natural selection may favor parents producing offspring with varying levels of plasticity. The current article presents a mathematical model assessing the logic of this hypothesis – specifically, it examines what conditions are required for natural selection to favor parents to bet‐hedge by varying their offspring's plasticity. Consistent with existing theory from biology, results show that between‐individual variation in plasticity cannot evolve when the environment only varies across space. If, however, the environment varies across time, selection can favor differential plasticity, provided fitness effects are large (i.e. variation in individuals’ plasticity is correlated with substantial variation in fitness). Our model also generates a novel restriction: Differential plasticity only evolves when the cost of being mismatched to the environment exceeds the benefits of being well matched. Based on mechanistic considerations, we argue that bet‐hedging by varying offspring plasticity, if it were to evolve, would be more likely instantiated via epigenetic mechanisms (e.g. pre‐ or postnatal developmental programming) than genetic ones (e.g. mating with genetically diverse partners). Our model suggests novel avenues for testing the bet‐hedging hypothesis of differential plasticity, including empirical predictions and relevant measures. We also discuss several ways in which future work might extend our model.
SP1 promotes the odontoblastic differentiation of dental papilla cells
Authors: Zhang Jie , Lin Heng , Liu Huan , Zhang Lu , Yuan Guohua , Chen Zhi 
Published: May 2015

Odontoblasts are a type of terminally differentiated and matrix‐secreting cells that are responsible for dentinogenesis. The process of odontoblast differentiation is regulated by a variety of transcription factors. The transcription factor SP1 is known to play an essential regulatory role in cell proliferation and differentiation. The purpose of this study was to investigate the role of SP1 in odontoblastic differentiation. Immunohistochemistry verified that SP1 was specifically expressed in polarizing and secretory odontoblasts in vivo. Quantitative reverse transcription–polymerase chain reaction (qRT–PCR) and immunofluorescence revealed that the expression of SP1 was significantly upregulated during odontoblastic differentiation of mDPC6T cells, a dental papilla cell line. Overexpression of SP1 significantly increased the expression of odontoblast‐related genes, including DSPP, DMP1 and ALP, and promoted the formation of mineralized nodules. Meanwhile, knockdown of SP1 decreased the expression of these odontoblast‐related genes and suppressed the formation of mineralized nodules. Our results demonstrate that SP1 promotes the odontoblastic differentiation and mineralization of dental papilla cells.
Salvage chemotherapy followed by granulocyte colony‐stimulating factor‐primed donor leukocyte infusion with graft‐vs.‐host disease control for minimal residual disease in acute leukemia/myelodysplastic syndrome after allogeneic hematopoietic stem cell transplantation: prognostic factors and clinical outcomes
Authors: Mo Xiao‐Dong , Zhang Xiao‐Hui , Xu Lan‐Ping , Wang Yu , Yan Chen‐Hua , Chen Huan , Chen Yu‐Hong , Han Wei , Wang Feng‐Rong , Wang Jing‐Zhi , Liu Kai‐Yan , Huang Xiao‐Jun 
Published: May 2015

AbstractThis study investigated the prognostic factors and clinical outcomes of preemptive chemotherapy followed by granulocyte colony‐stimulating factor‐primed donor leukocyte infusion (Chemo‐DLI) according to minimal residual disease (MRD) status in patients with acute leukemia and myelodysplastic syndromes who received allogeneic hematopoietic stem cell transplantation (HSCT) (n = 101). Patients received immunosuppressive drugs to prevent graft‐vs.‐host disease (GVHD) after Chemo‐DLI. The 3‐yr cumulative incidences of relapse, non‐relapse mortality, and disease‐free survival (DFS) afterHSCTwere 39.5%, 9.6%, and 51.7%, respectively. The cumulative incidences of relapse andDFSwere significantly poorer in patients who exhibited early‐onsetMRD. Forty‐four patients turnedMRDnegative 1 month after Chemo‐DLI; their cumulative incidences of relapse andDFSwere significantly better than those with persistentMRD1 month after preemptive Chemo‐DLI(relapse: 19.8% vs. 46.8%,P = 0.001;DFS: 69.6% vs. 46.4%,P = 0.004). The cumulative incidences of relapse andDFSafterHSCTwere significantly better in patients with chronicGVHD(cGVHD) than those withoutcGVHD(relapse: 19.6% vs. 63.7%,P < 0.001;DFS: 74.4% vs. 23.8%,P < 0.001). Early‐onsetMRD, persistentMRDafter Chemo‐DLI, and non‐cGVHDafter Chemo‐DLI, which were associated with increased relapse and impairedDFS, suggest unsatisfactory response to preemptive Chemo‐DLI.
Effects of elevated water temperature on physiological responses in adult freshwater mussels
Authors: Ganser Alissa M. , Newton Teresa J. , Haro Roger J. 
Published: May 2015

SummaryFreshwater mussels (order Unionoida) face multiple environmental stressors, which pose serious conservation challenges to this diverse assemblage of aquatic invertebrates. Of these stressors, elevated water temperature from global climate change and other anthropogenic sources may be the most ubiquitous and could be placing many mussel populations dangerously close to their thermal maxima.We tested the hypothesis that elevated water temperatures (20, 25, 30 and 35 °C) adversely affected physiological responses in adults of four North American species of mussels (Amblema plicata,Elliptio complanata, Fusconaia flavaandLampsilis cardium)in 21‐d laboratory tests.Oxygen consumption rates were directly affected by temperature inE. complanataandL. cardium, and indirectly affected by temperature inA. plicataandF. flava. Rates of O2consumption were generally positively correlated with water temperature. Ammonium excretion rates varied significantly with temperature inE. complanataand generally increased with temperature. The amount of O2consumed relative to nitrogen excreted (O : N ratio), varied significantly with temperature inA. plicata,E. complanataandF. flava. The tissue condition index varied among temperatures and species.These data suggest that elevated temperatures can alter metabolic rates in native mussels and may decrease the amount of energy that is available for key biological processes, such as survival, growth and reproduction.
Expression analysis of microRNA‐125 in patients with polycythemia vera and essential thrombocythemia and correlation with JAK2 allele burden and laboratory findings
Authors: Ferdowsi S. , Atarodi K. , Amirizadeh N. , Toogeh G. , Azarkeivan A. , Shirkoohi R. , Faranoush M. , Vaezi M. , Alimoghaddam K. , Ghavamzadeh A. , Naghadeh H. Teimori , Ghaffari S. H. 
Published: May 2015

SummaryIntroductionThe JAK2V617F mutation has emerged in recent years as a diagnostic as well as a treatment target in patients with polycythemia vera (PV) and essential thrombocythemia (ET). The disease phenotype is also influenced by other factors such as microRNA (miRNA) deregulation. The aim of this study was to investigate miR‐125 expression level in these patients with those obtained from healthy control subjects and its correlation with JAK2 allele burden and laboratory findings.MethodsIn total, forty patients with a clinical diagnosis of PV and ET were examined at the time of diagnosis. Ten healthy subjects were checked as controls. We performed JAK2 V617F allele burdens measurement and expression analysis of miR‐125b‐5p, miR‐125b‐3p, miR‐125a‐5p, and miR‐125a‐3p in leukocytes isolated from peripheral blood by quantitative real‐time polymerase chain reaction.ResultsMiR‐125b‐5p and miR‐125a‐5p were upregulated in both patients with PV (P = 0.00 and P = 0.003, respectively) and ET (P = 0.02 and P = 0.002, respectively). In PV group, a significant correlation was observed between miR‐125a‐5p and platelet counts (P = 0.01, r = 0.531). The correlation between miRNA and JAk2 allele burden was not significant.ConclusionIn conclusion, our data indicate that other factors such as aberrant miR‐125 expression may influence on the disease phenotype in patients with PV and ET.
Optogenetic versus electrical stimulation of dopamine terminals in the nucleus accumbens reveals local modulation of presynaptic release
Authors: Melchior James R. , Ferris Mark J. , Stuber Garret D. , Riddle David R. , Jones Sara R. 
Published: May 2015

AbstractThe nucleus accumbens is highly heterogeneous, integrating regionally distinct afferent projections and accumbal interneurons, resulting in diverse local microenvironments. Dopamine (DA) neuron terminals similarly express a heterogeneous collection of terminal receptors that modulate DA signaling. Cyclic voltammetry is often used to probe DA terminal dynamics in brain slice preparations; however, this method traditionally requires electrical stimulation to induce DA release. Electrical stimulation excites all of the neuronal processes in the stimulation field, potentially introducing simultaneous, multi‐synaptic modulation of DA terminal release. We used optogenetics to selectively stimulate DA terminals and used voltammetry to compare DA responses from electrical and optical stimulation of the same area of tissue around a recording electrode. We found that with multiple pulse stimulation trains, optically stimulated DA release increasingly exceeded that of electrical stimulation. Furthermore, electrical stimulation produced inhibition of DA release across longer duration stimulations. The GABAB antagonist, CGP 55845, increased electrically stimulated DA release significantly more than light stimulated release. The nicotinic acetylcholine receptor antagonist, dihydro‐β‐erythroidine hydrobromide, inhibited single pulse electrically stimulated DA release while having no effect on optically stimulated DA release. Our results demonstrate that electrical stimulation introduces local multi‐synaptic modulation of DA release that is absent with optogenetically targeted stimulation.
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The nucleus accumbens is highly heterogeneous, integrating regionally distinct afferent projections and accumbal interneurons, resulting in diverse microenvironments. Local electrical stimulation excites all of the neuronal processes in the stimulation field, potentially modulating the dopamine signal ‐ measured using cyclic voltammetry. Optogenetically targeting light stimulation to dopamine terminals (blue) reduces the cholinergic and GABAergic modulatory effects on stimulated dopamine release.
Feasibility study on the effectiveness of Goreisan‐based Kampo therapy for lower abdominal lymphedema after retroperitoneal lymphadenectomy via extraperitoneal approach
Authors: Komiyama Shinichi , Takeya Chiaki , Takahashi Rena , Yamamoto Yasuhiro , Kubushiro Kaneyuki 
Published: May 2015

AbstractAimTo evaluate the efficacy and safety of Kampo therapy based on Goreisan for lower abdominal lymphedema after surgical treatment of endometrial cancer or cervical cancer.MethodsRadical surgery, including retroperitoneal lymphadenectomy, was performed for endometrial cancer and cervical cancer. After surgery, Kampo therapy based on Goreisan and integrated physical therapy were provided for patients with lower abdominal lymphedema, especially lymphedema affecting the pubic‐inguinal‐vulval region. Goreisan (7.5g/day) was given orally three times a day (tds). If a significant response was not observed, Saireito (9 g/day; 3 g tds) or Gosyajinkigan (7.5 g/day; 2.5 g tds) was administered concomitantly.ResultsA total of 21 patients received treatment. The response rate to Goreisan monotherapy was 78%, with 22% being non‐responders. Median reduction of abdominal circumference was 2.1cm (95% CI 1.3‐2.85). When Goreisan was combined with another Kampo agent, the response rate was 92% and the non‐response rate was 8%. The median reduction of the abdominal circumference was 2.85 cm (95% CI: 2.25‐3.3). In particular, concomitant Goreisan and Saireito therapy achieved satisfactory results. No severe adverse reactions occurred.ConclusionsGoreisan‐based Kampo therapy might be effective and safe for lower abdominal lymphedema after retroperitoneal lymphadenectomy. We will perform a prospective control study in the near future.
Protective effect of melatonin‐supported adipose‐derived mesenchymal stem cells against small bowel ischemia‐reperfusion injury in rat
Authors: Chang Chia‐Lo , Sung Pei‐Hsun , Sun Cheuk‐Kwan , Chen Chih‐Hung , Chiang Hsin‐Ju , Huang Tien‐Hung , Chen Yi‐Ling , Zhen Yen‐Yi , Chai Han‐Tan , Chung Sheng‐Ying , Tong Meng‐Shen , Chang Hsueh‐Wen , Chen Hong‐Hwa , Yip Hon‐Kan 
Published: May 2015

AbstractWe tested the hypothesis that combined melatonin and autologous adipose‐derived mesenchymal stem cells (ADMSC) was superior to either alone against small bowel ischemia‐reperfusion (SBIR) injury induced by superior mesenteric artery clamping for 30 min followed by reperfusion for 72 hr. Male adult Sprague Dawley rats (n = 50) were equally categorized into sham‐operated controls SC, SBIR, SBIR‐ADMSC (1.0 × 106 intravenous and 1.0 × 106 intrajejunal injection), SBIR‐melatonin (intraperitoneal 20 mg/kg at 30 min after SI ischemia and 50 mg/kg at 6 and 18 hr after SI reperfusion), and SBIR‐ADMSC‐melatonin groups. The results demonstrated that the circulating levels of TNF‐α, MPO, LyG6+ cells, CD68+ cells, WBC count, and gut permeability were highest in SBIR and lowest in SC, significantly higher in SBIR‐ADMSC group and further increased in SBIR‐melatonin group than in the combined therapy group (all P < 0.001). The ischemic mucosal damage score, the protein expressions of inflammation (TNF‐α, NF‐κB, MMP‐9, MPO, and iNOS), oxidative stress (NOX‐1, NOX‐2, and oxidized protein), apoptosis (APAF‐1, mitochondrial Bax, cleaved caspase‐3 and PARP), mitochondrial damage (cytosolic cytochrome C) and DNA damage (γ‐H2AX) markers, as well as cellular expressions of proliferation (PCNA), apoptosis (caspase‐3, TUNEL assay), and DNA damage (γ‐H2AX) showed an identical pattern, whereas mitochondrial cytochrome C exhibited an opposite pattern compared to that of inflammation among all groups (all P < 0.001). Besides, antioxidant expressions at protein (NQO‐1, GR, and GPx) and cellular (HO‐1) levels progressively increased from SC to the combined treatment group (all P < 0.001). In conclusion, combined melatonin‐ADMSC treatment offered additive beneficial effect against SBIR injury.
Cerebral Cortical Microvascular Rarefaction in Metabolic Syndrome is Dependent on Insulin Resistance and Loss of Nitric Oxide Bioavailability
Authors: Chantler Paul D. , Shrader Carl D. , Tabone Lawrence E. , d'Audiffret Alexandre C. , Huseynova Khumara , Brooks Steven D. , Branyan Kayla W. , Grogg Kristin A. , Frisbee Jefferson C. 
Published: May 2015

AbstractObjectiveChronic presentation of the MS is associated with an increased likelihood for stroke and poor stroke outcomes following occlusive cerebrovascular events. However, the physiological mechanisms contributing to compromised outcomes remain unclear, and the degree of cerebral cortical MVD may represent a central determinant of stroke outcomes.MethodsThis study used the OZR model of MS and clinically relevant, chronic interventions to determine the impact on cerebral cortical microvascular rarefaction via immunohistochemistry with a parallel determination of cerebrovascular function to identify putative mechanistic contributors.ResultsOZR exhibited a progressive rarefaction (to ~80% control MVD) of the cortical microvascular networks vs. lean Zucker rats. Chronic treatment with antihypertensive agents (captopril/hydralazine) had limited effectiveness in blunting rarefaction, although treatments improving glycemic control (metformin/rosiglitazone) were superior, maintaining ~94% control MVD. Chronic treatment with the antioxidant TEMPOL severely blunted rarefaction in OZR, although this ameliorative effect was prevented by concurrent NOS inhibition.ConclusionsFurther analyses revealed that the maintenance of glycemic control and vascular NO bioavailability were stronger predictors of cerebral cortical MVD in OZR than was prevention of hypertension, and this may have implications for chronic treatment of CVD risk under stroke‐prone conditions.
Effects of Cognitive Behavioral Stress Management on Negative Mood and Cardiac Autonomic Activity in ICD Recipients
Authors: RUSSELL DOUGLAS C. , SMITH TRACEY L. , KRAHN DEAN D. , GRASKAMP PETER , SINGH DALIP , KOLDEN GREGORY G. , SIGMUND HEIDI , ZHANG ZHENGJUN 
Published: May 2015

BackgroundBehavioral intervention studies in patients with an implantable cardioverter‐defibrillator (ICD) show promise in improving psychosocial outcomes but inconclusive effects on cardiovascular outcome. We assessed the effects of cognitive behavioral stress management (CBSM) on mood state and potentially arrhythmogenic cardiovascular responses to mental stress in ICD patients, in support of further larger scale arrhythmia trials.MethodsA total of 103 ICD recipients were randomly assigned to 10‐week programs of CBSM or “Patient Education” (ED). Of these, 83 patients continued to either CBSM (n = 44) or ED (n = 39) intervention. Study end points were mood change, heart rate variability (HRV), double product elevation (DP = heart rate × systolic blood pressure) by math and anger‐recall stress, and arrhythmia up to 6 months follow‐up.ResultsAdjusting for multiple testing, CBSM was associated with moderate effect size reductions in tension/anxiety (P = 0.010), anger/hostility (P = 0.020), perceived stress (P = 0.037), and total mood disturbance (P = 0.025), greatest immediately following intervention (P < 0.05), and partially attributable to increased negative mood following ED (P < 0.01). No significant intervention effects on high frequency or low frequency spectral power of HRV, DP responses, or cardiac arrhythmias were demonstrated.ConclusionsCBSM intervention in ICD recipients resulted in reduced anxiety, anger, and perceived stress, not sustained at 6 months follow‐up, and without conclusive effect on cardiac autonomic or hemodynamic responses to mental stress, or arrhythmia. Findings support conduct of larger behavioral intervention arrhythmia trial, with consideration of reinforcement training and targeting of subgroup responders to therapy.
Interruption of Pacing Following Nonsustained Ventricular Tachycardia in an AAI Programmed Implantable Cardioverter Defibrillator
Authors: Egan Paul , Wilkoff Bruce L. , Tchou Patrick 
Published: May 2015

BackgroundUnnecessary ventricular pacing from cardiac implantable electronic devices has been associated with long‐term risks (heart failure, atrial fibrillation, and possibly stroke). Several device programming strategies are available to minimize ventricular pacing, each potentially associated with unintended consequences. Occasionally, the only effective means is to program to the AAI(R) pacing mode. However, in one manufacturer's implantable cardioverter defibrillators (ICDs), the AAI(R) mode has the potential risk of prolonged pacing cessation following a nonsustained ventricular tachycardia (NSVT).MethodPatients with ICDs, managed through the Cleveland Clinic device clinic, follow the Heart Rhythm Society consensus document recommendations for device monitoring with remote interrogations (every three months) and yearly in‐person evaluations. Clinically significant findings also trigger additional evaluations by the nurse and physician.ResultsTwo patients having Boston Scientific ICDs (E110 Teligen 100; Boston Scientific Corp., Natick, MA, USA), had asystole and marked bradycardia following untreated NSVT. These pauses in pacing were due to use of the AAI(R) pacing mode. In order to enhance ventricular tachycardia detection, by design atrial pacing is disabled during, and for a time after, an episode of ventricular tachycardia when the device operates in the “ventricular tachycardia response” (VTR) phase. Thus, following spontaneous termination of the NSVT, no pacing occurred in these patients until the VTR period ended. Nonconventional programming was utilized to permit AAI(R) pacing while avoiding these asystolic and bradycardic events during VTR.ConclusionsUnintended consequences can occur when complex VT detection parameters interact with specific pacing modes. At times, nonconventional programming can avoid these interactions while still achieving effective AAI(R) pacing.
Schadenfreude as a mate‐value‐tracking mechanism: Replication and extension of Colyn and Gordon (2013)
Authors: VAN DIJK WILCO W. , OUWERKERK JAAP W. , SMITH RICHARD H. 
Published: May 2015

AbstractThe present research provides a replication and extension of L. A. Colyn and A. K. Gordon's (2013) study on gender differences in schadenfreude. An experiment—in which both the gender of the unfortunate other and the dimension on which the misfortune occurred were manipulated—showed that female participants reported more schadenfreude when a same‐gender other (vs. an opposite‐gender other) experienced a misfortune on the dimension of physical attractiveness (vs. social status), whereas male participants reported more schadenfreude when a same‐gender other (vs. an opposite‐gender other) experienced a misfortune on the dimension of social status (vs. physical attractiveness). In the discussion, differences between our results and those of Colyn and Gordon are discussed.