bluuebunny/crossref_metadata_2025_split huggingface dataset:
Olfactory Acuity in Chronic Migraine: A Cross‐Sectional Study
Authors: Whiting Alexander C. , Marmura Michael J. , Hegarty Sarah E. , Keith Scott W. 
Published: November 2014

Objective/BackgroundThis study aims to measure olfactory acuity in chronic migraine subjects, at baseline and on migraine days, and compare to age‐ and sex‐matched controls. Olfactory impairment is common in neurological disorders. While smell hypersensitivity has been established with chronic migraine, olfactory acuity has not been well studied.MethodsWe recruited 50 subjects with chronic migraine from the Jefferson Headache Center and 50 age‐ and sex‐matched controls. Using the University of Pennsylvania Smell Identification Test (UPSIT), a validated test of olfaction, olfactory acuity was measured at baseline and during a migraine for subjects, and compared to controls at baseline and at home 2 weeks later. All subjects were additionally screened for odor sensitivity and allodynia.ResultsThe mean UPSIT score for migraine subjects was 34.5 on non‐migraine days and 34.7 on migraine days (mean difference = −0.4, 95% confidence interval [CI; −1.3, 0.6] P = .45). Controls had a mean of 35.9 and 36.1 for each test day (mean difference = −0.1, 95% CI [−0.9, 0.7] P = .87). On average, migraineurs performed worse than their matched control counterparts in both test sittings (test 1: P = .047; test 2: P = .01). The great majority of subjects were allodynic (42/50) compared with only 9 of 50 controls, and the majority of subjects (41/50) found more than one listed odor to be bothersome, compared with only 10/50 controls. On non‐migraine days, 18/48 chronic migraine subjects had abnormal olfaction and on migraine days 14/42 had abnormal olfaction, compared with only 9/50 controls who had abnormal olfaction on their first UPSIT.ConclusionsWhile chronic migraine patients do not appear to have a significant change in olfactory acuity between migrainous and non‐migrainous periods, they do appear to be more likely to have abnormal olfactory acuity at baseline compared to age‐ and sex‐matched controls.
Stevens–Johnson syndrome and toxic epidermal necrolysis: a 20‐year single‐center experience
Authors: Lalosevic Jovan , Nikolic Milos , Gajic‐Veljic Mirjana , Skiljevic Dusan , Medenica Ljiljana 
Published: November 2014

AbstractBackgroundStevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life‐threatening diseases that are most frequently caused by drugs.ObjectivesThe purpose of this study was to summarize 20 years of experience with SJS and TEN in the largest dermatology clinic in Serbia.MethodsThe study included 38 patients treated during the period 1993–2012. The patients were classified into three groups according to whether they were diagnosed with SJS, a condition representing an overlap of SJS and TEN (SJS/TEN), or TEN. Patients with TEN were also divided into three groups according to the modality of therapy: supportive therapy (ST) only (n = 3); ST plus systemic corticosteroids (SC) (n = 8); and ST plus SC plus IV immunoglobulins (IVIG) (n = 6).ResultsThe study population included 13 SJS patients, eight SJS/TEN patients, and 17 TEN patients. The disease had started at a mean ± standard deviation (SD) of 7.1 ± 3.5 days after the commencement of treatment with the offending drug. The disease resulted in three lethal outcomes, all of which occurred in TEN patients. However, the predicted mortality for the whole group was 5.6 in 38 patients, whereas that for the TEN group was 3.97 in 17 patients. The differences between actual and predicted rates of mortality were not significant. Among the three groups of TEN patients, there were no significant differences in the commencement of re‐epithelialization or the duration of hospitalization.ConclusionsIn the present study, nonsteroidal anti‐inflammatory and anti‐infective drugs were the most frequent causative agents (eight patients in each group). In the group of SJS and SJS/TEN patients treated with ST and SC, the mortality rate was 0%. In TEN patients, the mortality rate was 17.6% (three of 17 patients). There were no significant differences in mortality rate among the three TEN treatment groups, but the results may have been biased by the small number of patients.
Impact of enforcing a statutory minimum wage on work and quality of life of vulnerable groups in Hong Kong
Authors: Wong Hung , Ye Shengquan 
Published: November 2014

The statutory minimum wage (SMW) law was enforced in Hong Kong on 1 May 2011. To examine its impact, this longitudinal study measured the quality of life, job and pay satisfaction, monthly income, hourly rate and working hours of vulnerable groups (n = 253) before and after the legislation. The findings confirmed that the enforcement of the SMW induced a positive impact as intended. The introduction of the SMW induced a positive wage and employment effect on the vulnerable groups in Hong Kong without harming their employment rate. Job and pay satisfaction, as well as most domains of the quality of life (i.e., physical and psychological health, and environment), increased significantly. In general, the positive impact of the SMW was more prominent for employees who previously worked less than 18 hours a week and who had hourly rates less than 28 HKD. The implications of the findings are discussed in the social context of Hong Kong.Key Practitioner Message: ● Enforcing minimum wage induced a positive impact on quality of life, job and pay satisfaction, and a monthly income of vulnerable groups. ● The social relations (quality of life) decreased after implementing minimum wage for workers working longer than 18 hours a week. ● Longer working hours is a key factor for the increase of a monthly income among the vulnerable groups.
Transgenic characterization of two testis‐specific promoters in the silkworm, Bombyx mori
Authors: Xu J. , Bi H. , Chen R. , Aslam A. F. M. , Li Z. , Ling L. , Zeng B. , Huang Y. , Tan A. 
Published: November 2014

AbstractSex‐specific regulatory elements are key components for developing insect genetic sexing systems. The current insect genetic sexing system mainly uses a female‐specific modification system whereas little success was reported on male‐specific genetic modification. In the silkworm Bombyx mori, a lepidopteran model insect with economic importance, a transgene‐based, female‐specific lethality system has been established based on sex‐specific alternative splicing factors and a female‐specific promoter BmVgp (vitellogenin promoter) has been identified. However, no male‐specific regulatory elements have yet been identified. Here we report the transgenic identification of two promoters that drive reporter gene expression in a testis‐specific manner in B. mori. Putative promoter sequences from the B. mori Radial spoke head 1 gene (BmR1) and beta‐tubulin 4 gene (Bmβ4) were introduced using piggybac‐based germline transformation. In transgenic silkworms, expression of the reporter gene enhanced green fluorescent protein (EGFP) directed by either BmR1 promoter (BmR1p) or Bmβ4p showed precisely testis‐specific manners from the larval to adult stage. Furthermore, EGFP expression of these two transgenic lines showed different localization in the testis, indicating that BmR1p or Bmβ4p might be used as distinct regulatory elements in directing testis‐specific gene expression. Identification of these testis‐specific promoters not only contributes to a better understanding of testis‐specific gene function in insects, but also has potential applications in sterile insect techniques for pest management.
A few steps forward and no steps back: long‐distance dispersal patterns in small carpenter bees suggest major barriers to back‐dispersal
Authors: Rehan Sandra , Schwarz Michael 
Published: November 2014

AbstractAimInequality between rates of forward and backward dispersal is one mechanism that will produce regional differences in biotic composition. Any such differences will affect ecosystem assembly. Thus, it is important to understand why unequal dispersal rates might occur. Recent studies have indicated strong differences between forward and backward dispersal in two major bee groups, Hylaeinae and Allodapini. Here, we use a third bee group, tribe Ceratinini, to determine whether this might be a more general phenomenon.LocationWorldwide.MethodsCeratinini is globally distributed (excepting Antarctica) and contains the single genus Ceratina and 21 subgenera, most of which are endemic to continents. We examined the phylogeny of Ceratinini using sequence data from three genes and 99 species, and inferred ancestral distributions using Bayesian and maximum likelihood approaches.ResultsWe show that the tribe Ceratinini had an African origin in the early Eocene. This was followed by four dispersals out of Africa in the Eocene and early Oligocene and three further dispersals between the Miocene and the present. There has been no back‐dispersal of Ceratinini to Africa. The lack of back‐dispersal cannot be explained by species abundance in non‐African regions, and physical barriers to back‐dispersal seem unlikely.Main conclusionsOur results are similar to findings for two other major bee groups and indicate that back‐dispersal is very rare. It is unlikely that physical barriers can explain these patterns. However, dispersal patterns might be explained by assembly rules such as niche pre‐emption or by reduced opportunities for escaping into enemy‐free space. At a continental level, it is likely that the composition of bee fauna is more strongly influenced by very early dispersal events rather than by later physical barriers to dispersal.
Pleistocene speciation is not refuge speciation
Authors: Rull Valentí 
Published: November 2014

AbstractA number of researchers working on the origin of extant Neotropical biodiversity implicitly and without appropriate proofs assume that Pleistocene speciation should necessarily follow the rules of the refuge hypothesis. A recent example is provided by a study of Neotropical butterflies. Although the analysis showed that these groups experienced their main diversification burst during the last 2.6 million years, coinciding with the Pleistocene glacial cycles (Garzón‐Orduña et al., 2014, Journal of Biogeography, 41, 1631–1638), a causal link between the speciation chronology and the evolutionary mechanisms proposed by the refuge hypothesis is not provided. Without more detailed studies on the environmental drivers, geographical patterns and speciation modes, establishing a causal link between speciation chronology and a particular speciation model – of which the refuge hypothesis is only one among many possibilities – is too speculative. Here I provide a six‐step conceptual framework for linking the speciation chronology with the environmental drivers and the ecological and evolutionary mechanisms potentially involved.
Hypothesis: cell signalling influences age‐related risk of colorectal cancer
Authors: Bordonaro Michael , Lazarova Darina L. 
Published: November 2014

AbstractWe propose that ageing is linked to colonic carcinogenesis through crosstalk between Wnt activity and signalling pathways related to ageing and senescence: progerin, klotho and mTOR. Mutations in the Wnt signalling pathway are responsible for the majority of colorectal cancers (CRCs); however, hyperactivation of Wnt signalling by butyrate, a breakdown product of dietary fibre, induces CRC cell apoptosis. This effect of butyrate may in part explain the protective action of fibre against CRC. Hutchinson–Gilford progeria syndrome is a premature ageing disorder caused by accumulation of the progerin protein; however, healthy individuals also produce progerin in the course of their normal ageing. Progerin activates expression of the Wnt inhibitors HES1 and TLE1. Thus, we hypothesize that with age, the increasing expression of progerin suppresses butyrate‐mediated Wnt hyperactivation and apoptosis, leading to increased CRC risk. Wild‐type klotho contributes to a significantly increased lifespan; however, Klotho gene variants differ significantly between newborns and elderly. Klotho inhibits basal Wnt signalling activity; thus, the protein may function as a tumour suppressor for CRC. However, similar to progerin, klotho variants associated with lifespan differences may repress butyrate‐mediated Wnt hyperactivation, and thus increase the risk of CRC. Finally, mTOR signalling has also been linked to human ageing, and crosstalk between Wnt and mTOR signalling may influence colonic tumourigenesis. Understanding how progerin, klotho and mTOR link ageing with colonic neoplastic development may lead to novel preventive and therapeutic strategies against CRC associated with age.
Role of p38 MAPK in enhanced human cancer cells killing by the combination of aspirin and ABT‐737
Authors: Zhang Chong , Shi Jing , Mao Shi‐ying , Xu Ya‐si , Zhang Dan , Feng Lin‐yi , Zhang Bo , Yan You‐you , Wang Si‐cong , Pan Jian‐ping , Yang You‐ping , Lin Neng‐ming 
Published: November 2014

AbstractRegular use of aspirin after diagnosis is associated with longer survival among patients with mutated‐PIK3CA colorectal cancer, but not among patients with wild‐type PIK3CA cancer. In this study, we showed that clinically achievable concentrations of aspirin and ABT‐737 in combination could induce a synergistic growth arrest in several human PIK3CA wild‐type cancer cells. In addition, our results also demonstrated that long‐term combination treatment with aspirin and ABT‐737 could synergistically induce apoptosis both in A549 and H1299 cells. In the meanwhile, short‐term aspirin plus ABT‐737 combination treatment induced a greater autophagic response than did either drug alone and the combination‐induced autophagy switched from a cytoprotective signal to a death‐promoting signal. Furthermore, we showed that p38 acted as a switch between two different types of cell death (autophagy and apoptosis) induced by aspirin plus ABT‐737. Moreover, the increased anti‐cancer efficacy of aspirin combined with ABT‐737 was further validated in a human lung cancer A549 xenograft model. We hope that this synergy may contribute to failure of aspirin cancer therapy and ultimately lead to efficacious regimens for cancer therapy.
Sitagliptin attenuates sympathetic innervation via modulating reactive oxygen species and interstitial adenosine in infarcted rat hearts
Authors: Lee Tsung‐Ming , Chen Wei‐Ting , Yang Chen‐Chia , Lin Shinn‐Zong , Chang Nen‐Chung 
Published: November 2014

AbstractWe investigated whether sitagliptin, a dipeptidyl peptidase‐4 (DPP‐4) inhibitor, attenuates arrhythmias through inhibiting nerve growth factor (NGF) expression in post‐infarcted normoglycemic rats, focusing on adenosine and reactive oxygen species production. DPP‐4 bound adenosine deaminase has been shown to catalyse extracellular adenosine to inosine. DPP‐4 inhibitors increased adenosine levels by inhibiting the complex formation. Normoglycemic male Wistar rats were subjected to coronary ligation and then randomized to either saline or sitagliptin in in vivo and ex vivo studies. Post‐infarction was associated with increased oxidative stress, as measured by myocardial superoxide, nitrotyrosine and dihydroethidium fluorescent staining. Measurement of myocardial norepinephrine levels revealed a significant elevation in vehicle‐treated infarcted rats compared with sham. Compared with vehicle, infarcted rats treated with sitagliptin significantly increased interstitial adenosine levels and attenuated oxidative stress. Sympathetic hyperinnervation was blunted after administering sitagliptin, as assessed by immunofluorescent analysis and western blotting and real‐time quantitative RT‐PCR of NGF. Arrhythmic scores in the sitagliptin‐treated infarcted rats were significantly lower than those in vehicle. Ex vivo studies showed a similar effect of erythro‐9‐(2‐hydroxy‐3‐nonyl) adenine (an adenosine deaminase inhibitor) to sitagliptin on attenuated levels of superoxide and NGF. Furthermore, the beneficial effects of sitagliptin on superoxide anion production and NGF levels can be reversed by 8‐cyclopentyl‐1,3‐dipropulxanthine (adenosine A1 receptor antagonist) and exogenous hypoxanthine. Sitagliptin protects ventricular arrhythmias by attenuating sympathetic innervation via adenosine A1 receptor and xanthine oxidase‐dependent pathways, which converge through the attenuated formation of superoxide in the non‐diabetic infarcted rats.
Connexin 31.1 degradation requires the Clathrin‐mediated autophagy in NSCLC cell H1299
Authors: Zhu Xingli , Ruan Zhenchao , Yang Xiufang , Chu Kaili , Wu Hai , Li Yao , Huang Yan 
Published: November 2014

AbstractConnexins have relative short half‐lives. Connexin 31.1 (Cx31.1) was newly reported to be down‐regulated in non‐small cell lung cancer cell lines, and displayed tumour‐suppressive properties. However, no reports describing how a cell regulates Cx31.1 level were found. In this study, Cx31.1 was suggested to be degraded through both ubiquitin–proteasome system (UPS) and autophagy. Blockage of UPS with MG‐132 increased Cx31.1 level, but could not inhibit the degradation of Cx31.1 completely. In H1299 cells stably expressing Cx31.1, Cx31.1 reduced when autophagy was induced through starvation or Brefeldin A treatment. Knockdown of autophagy‐related protein ATG5 could increase the cellular level of Cx31.1 both under normal growth condition and starvation‐induced autophagy. Colocalization of Cx31.1 and autophagy marker light chain 3 (LC3) was revealed by immunofluorescence analysis. Coimmunoprecipitation and immunofluorescence showed that Cx31.1 might interact with clathrin heavy chain which was newly reported to regulate autophagic lysosome reformation (ALR) and controls lysosome homoeostasis. When clathrin expression was knockdown by siRNA treatment, the level of Cx31.1 increased prominently both under normal growth condition and starvation‐induced autophagy. Under starvation‐induced autophagy, LC3‐II levels were slightly accumulated with siCla. treatment compared to that of siNC, which could be ascribed to that clathrin knockdown impaired the late stage of autophagy, ALR. Taken together, we found autophagy contributed to Cx31.1 degradation, and clathrin might be involved in the autophagy of Cx31.1.
Acroosteolysis presenting with brachyonychia following exposure to cold
Authors: EL‐Komy M.H.M. , Baran R. 
Published: November 2014

AbstractBackgroundA vast number of conditions ranging from simple trauma to hereditary and collagen vascular disease had been described in association with acroosteolysis.ObjectiveTo demonstrate that severe cold exposure not mounting to frostbite may be associated with acroosteolysis.MethodsA 16–year‐old girl with acroosteolysis presenting with brachyonychia was fully investigated for possible cause of her nail and bone deformity.ResultsLab investigations including Parathormone levels, Anti Scl 70, ANA, Anti‐CCP and RF levels were all normal. X‐ray imaging revealed resorption of the tufts of the terminal phalanges bilaterally. Disruption of nail fold capillaries with sluggish flow in capillary loops was evident on capillaroscopy.ConclusionIt had been repeatedly reported that frostbite, Raynaud's disease and diseases associated with repeated chilblains may be associated with secondary cold‐induced acroosteolysis. Here, we present a case of acroosteolysis associated with brachyonychia following exposure to severe cold not mounting to frostbite.
Impact of brief and sequential exposure to nystatin, amphotericin B, ketoconazole, and fluconazole in modulating adhesion traits of oral Candida dubliniensis isolates
Authors: Ellepola Arjuna N.B. , Joseph Bobby K. , Samaranayake Lakshman P. , Bandara H.M.H.N. , Khan Zia U. 
Published: November 2014

AbstractAimCandida adherence is implicated in the pathogenesis of oral candidosis. Adhesion to buccal epithelial cells (BEC), germ tube (GT) formation, and relative cell surface hydrophobicity (CSH) are colonization attributes of candidal pathogenicity. Candida dubliniensis (C. dubliniensis) is allied with recurrent oral candidosis, which can be treated with nystatin, amphotericin B, ketoconazole, and fluconazole. Due to the diluent effect of saliva and the cleansing effect of the oral musculature in the oral cavity C. dubliniensis isolates undergo brief and sequential exposure to antifungal agents during therapy. Thus, in the present study, we evaluated the adhesion to BEC, GT formation, and the CSH of oral isolates of C. dubliniensis following brief and sequential exposure to nystatin, amphotericin B, ketoconazole, and fluconazole.MethodsAfter determining the minimum inhibitory concentration (MIC) of the aforementioned drugs, 20 oral isolates of C. dubliniensis were briefly (1 h), and sequentially (10 days) exposed to subcidal concentrations of these drugs. Following drug removal, adhesion to BEC, GT formation, and CSH of these isolates were determined.ResultsThe percentage reduction of adhesion to BEC, GT formation, and CSH of the isolates following exposure to antifungal agents were as follows: nystatin: 53.55%, 33.98%, and 29.83% (P < 0.001); amphotericin B: 53.84%, 36.23%, and 28.97% (P < 0.001); ketoconazole: 37.43%, 20.51%, and 16.49% (P < 0.001); and fluconazole: 8.93% (P < 0.001), 1.6%, and 0.63% (P > 0.05).ConclusionsBrief and sequential exposure of C. dubliniensis to antifungal agents would continue to wield an antifungal effect by altering its adhesion attributes, and elucidate possible pharmacodynamics by which antifungal agents might operate in modulating candidal adherence.
The Wax and Wane of Narcissism: Grandiose Narcissism as a Process or State
Authors: Giacomin Miranda , Jordan Christian H. 
Published: November 2014

AbstractThough grandiose narcissism has predominantly been studied in structural terms—focused on individuals' general tendencies to be more or less narcissistic—we tested whether it also has a meaningful process or state component. Using a daily diary study methodology and multilevel modeling (N = 178 undergraduates, 146 female; Mage = 18.86, SD = 2.21), we examine whether there is significant variability in daily state narcissism and whether this variability relates systematically to other psychological states (i.e., self‐esteem, stress) and daily events. We assessed state narcissism and daily experiences over a 10‐day period. We observed significant within‐person variability in daily narcissism. Notably, this variability was not simply random error, as it related systematically to other psychological states and daily events. Specifically, state narcissism was higher when people experienced more positive agentic outcomes (e.g., having power over someone) or more positive communal outcomes (e.g., helping someone with a problem). State narcissism was lower on days people experienced greater felt stress. These relations held when state self‐esteem, gender, and trait narcissism were controlled. These findings suggest that grandiose narcissism has a meaningful process or state component.