bluuebunny/crossref_metadata_2025_split huggingface dataset:
Management of Pediatric Migraine Headache in the Emergency Room and Infusion Center
Authors: Kabbouche Marielle 
Published: October 2015

Migraine is a common disorder that starts at an early age and takes a variable pattern from intermittent to chronic headache with several exacerbations throughout a lifetime.Children and adolescents are significantly affected. If an acute headache is not aborted by outpatient migraine therapy, it often causes severe disability, preventing the child from attending school and social events. Treating the acute severe headache aggressively helps prevent prolonged disability as well as possible chronification.Multiple medications are available, mostly for the outpatient management of an attack and include the use of over‐the‐counter anti‐inflammatory medications as well as prescribed medications in the triptan group. These therapies do sometime fail and the exacerbation can last from days to weeks. If the headache lasts 72 hours or longer it will fall in the category of status migrainosus. Status migrainosus is described as a severe disabling headache lasting 72 hours or more by the ICHD3 criteria. Disability is a major issue in children and adolescents and aggressive acute measures are to be taken to control it as soon as possible. Early aggressive intravenous therapy can be very effective in breaking the attack and allowing the child to be quickly back to normal functioning.This article reviews what is available for the treatment of pediatric primary headaches in the emergency room.
Industry Expertise, Information Leakage and the Choice of M&A Advisors
Authors: Chang Xin , Shekhar Chander , Tam Lewis H. K. , Yao Jiaquan 
Published: October 2015

AbstractThis paper examines the impacts of M&A advisors’ industry expertise on firms’ choice of advisors in mergers and acquisitions. We show that an investment bank's expertise in merger parties’ industries increases its likelihood of being chosen as an advisor, especially when the acquisition is more complex, and when a firm in M&A has less information about the merger counterparty. However, due to the concerns about information leakage to industry rivals through M&A advisors, acquirers are reluctant to share advisors with rival firms in the same industry, and they are more likely to switch to new advisors if their former advisors have advisory relationship with their industry rivals. In addition, we document that advisors with more industry expertise earn higher advisory fees and increase the likelihood of deal completion.
Influence of CYP2D6 and β2‐adrenergic receptor gene polymorphisms on the hemodynamic response to propranolol in Chinese Han patients with cirrhosis
Authors: Zhang Feng , Duan Xuhong , Zhang Ming , Li Zhenlei , He Qibin , Wang Yi , Miao Chengcheng , Zhong Wenqi , Zou Xiaoping , Zhuge Yuzheng 
Published: October 2015

AbstractBackground and AimPropranolol is widely used to prevent gastroesophageal variceal bleeding; however, some patients could not benefit from propranolol. This study is to evaluate the relationship between CYP2D6 and β2‐adrenergic receptor (β2‐AR) gene polymorphisms and the hemodynamic response to propranolol in Chinese Han patients.MethodsThe clinical data of patients with gastroesophageal varices undergoing hepatic venous pressure gradient (HVPG) measurement before and 7 days after oral propranolol administration in our department were collected. Four single nucleotide polymorphisms of CYP2D6 and β2‐AR genes were detected. The relationship was identified by logistic regression model.ResultsThirty patients were involved in the analysis. Sixty milligram propranolol twice each day was well tolerated by all the patients. The initial and secondary average of HVPG was 17.4 ± 5.8 mmHg vs. 13.2 ± 4.8 mmHg, respectively (t = 5.726, P < 0.001). Twenty patients responded to propranolol. The mean reduction value of HVPG was 6.6 ± 3.6 mmHg (range from 3 to 19). Genotype analysis showed: 20 homozygotes for C/C188 and 10 for heterozygous C/T188, 8 homozygotes for G/G4268 and 22 heterozygotes for G/C4268, 14 homozygotes for Gly16 and 10 heterozygotes, and 6 homozygotes for Arg16, 27 homozygotes for Gln27 and 3 heterozygotes. The multivariate logistic regression analysis indicated that CYP2D6 (188C>T) genotype was an independent predicting factor for HVPG response to propranolol (P = 0.033).ConclusionsCYP2D6 (188C>T) gene polymorphisms influence the hemodynamic response to propranolol in this population of Chinese Han patients with gastroesophageal varices. However, HVPG response cannot be completely predicted from CYP2D6 and β2‐AR gene polymorphisms.
LncRNA‐ATB mediated E‐cadherin repression promotes the progression of colon cancer and predicts poor prognosis
Authors: Yue Ben , Qiu Shenglong , Zhao Senlin , Liu Chenchen , Zhang Dongyuan , Yu Fudong , Peng Zhihai , Yan Dongwang 
Published: October 2015

AbstractBackgroundLong non‐coding RNA‐activated by TGF‐β (lncRNA‐ATB) promotes the invasion–metastasis cascade in hepatocellular carcinoma via downregulating E‐cadherin (E‐cad) and inducing epithelial‐to‐ mesenchymal transition (EMT) and is clinically significant in human colon cancer. However, its molecular mechanisms in colon cancer progression remain unclear. This study aimed to elucidate the role of lncRNA‐ATB and its clinical value in colon cancer.MethodsExpression levels of lncRNA‐ATB in colon cancer tissues and colon cancer cell lines were evaluated using quantitative real‐time polymerase chain reaction. The clinicopathological significance and prognostic value of lncRNA‐ATB were investigated, and roles of lncRNA‐ATB in regulating E‐cad and other EMT‐related markers expression and colon cancer progression were evaluated in vitro. Expression levels of lncRNA‐ATB and E‐cad in human plasma were evaluated.ResultsLong non‐coding RNA‐activated by TGF‐β was upregulated in colon cancer tissues compared with adjacent mucosa (P < 0.001). LncRNA‐ATB levels were also higher in metastatic cancer tissues (P < 0.001). Among the three highly invasive colon cancer cell lines, lncRNA‐ATB levels were relatively higher with concurrent low levels of E‐cad compared with levels in the three low‐invasive cell lines. LncRNA‐ATB expression correlated with pN stage (P < 0.01) and American Joint Committee on Cancer stage (P < 0.01). Striking differences were observed in overall survival and disease‐free survival in cases with both high lncRNA‐ATB expression and low E‐cad expression. Reduction of lncRNA‐ATB increased expression of epithelial markers E‐cad, ZO‐1, and decreased expression of mesenchymal markers ZEB1 and N‐cadherin (N‐cad), and significantly influenced colon cancer cell progression. Plasma lncRNA‐ATB was upregulated in colon cancer patients one month after surgery (P < 0.05).ConclusionsLong non‐coding RNA‐activated by TGF‐β may act on colon tumorigenesis by suppressing E‐cad expression and promoting EMT process, and lncRNA‐ATB inhibition may provide a promising therapeutic option for suppressing colon cancer progression.
The pleiotropic ABNORMAL FLOWER AND DWARF1 affects plant height, floral development and grain yield in rice
Authors: Ren Deyong , Rao Yuchun , Wu Liwen , Xu Qiankun , Li Zizhuang , Yu Haiping , Zhang Yu , Leng Yujia , Hu Jiang , Zhu Li , Gao Zhenyu , Dong Guojun , Zhang Guangheng , Guo Longbiao , Zeng Dali , Qian Qian 
Published: October 2015

AbstractModerate plant height and successful establishment of reproductive organs play pivotal roles in rice grain production. The molecular mechanism that controls the two aspects remains unclear in rice. In the present study, we characterized a rice gene, ABNORMAL FLOWER AND DWARF1 (AFD1) that determined plant height, floral development and grain yield. The afd1 mutant showed variable defects including the dwarfism, long panicle, low seed setting and reduced grain yield. In addition, abnormal floral organs were also observed in the afd1 mutant including slender and thick hulls, and hull‐like lodicules. AFD1 encoded a DUF640 domain protein and was expressed in all tested tissues and organs. Subcellular localization showed AFD1‐green fluorescent fusion protein (GFP) was localized in the nucleus. Meantime, our results suggested that AFD1 regulated the expression of cell division and expansion related genes.
Evaluation of Mandibular Movement Functions Using Instrumental Ultrasound System
Authors: Sójka Anna , Huber Juliusz , Kaczmarek Elżbieta , Hędzelek Wiesław 
Published: October 2015

AbstractPurposeThe article deals with routinely performed instrumental temporomandibular joint (TMJ) examinations and interpretation of findings obtained from the Arcus Digma ultrasound device in individuals with or without clinical symptoms of temporomandibular disorders (TMD). The aim of this study was to analyze mandibular movement functions and the relationship between incisors and condylar movement parameters during jaw opening, which may be helpful for clinical evaluation in these patients.Materials and methodsThe study group consisted of 84 young students with no dental problems and other serious acute or chronic diseases in the medical history; the students were examined both clinically and with the Arcus Digma ultrasound device.ResultsHelkimo Di = I was the most common score in 49 participants, and Helkimo Di = II in a significantly (p < 0.01, Di = I vs. Di = II) smaller number of participants. Medical history revealed symptoms of unilateral mastication in 15 participants and a statistically significant increased (p < 0.02, participants with symptoms of unilateral mastication vs. asymptomatic) condylar range of motion parameter during retrusion. Also a significant decrease (p < 0.03, participants with symptoms of unilateral mastication vs. asymptomatic) of the incisal and condylar ranges of motion during mouth opening was found. Limitation of mouth opening, defined as a decrease of inter‐incisal distance, appeared in 19 participants (22.6%) and in 25 participants (29.8%) measured instrumentally with the Arcus Digma device. A comparison of instrumental result examinations of the right and left TMJs showed positive correlations of the range of mandible opening movement with the Posselt opening movement (r = 0.75) and opening/closing movements with the Posselt closing movements (r = 0.70). A correlation was demonstrated (r = 0.81) between the condylar range of motion studied on the left and on the right TMJ during mandible opening movement. Correlations were also found between opening‐closing movements and the condylar range of motion of the left TMJ, and between the opening‐closing movement and the condylar range of motion of the right TMJ during the opening movement.ConclusionsAccording to the results of this study with instrumental Arcus Digma ultrasound device measurements of mandibular movements, data were provided on irregularities in TMJ function not detected in participants with or without clinical symptoms of TMD.
Burn depth assessments by photoacoustic imaging and laser Doppler imaging
Authors: Ida Taiichiro , Iwazaki Hideaki , Kawaguchi Yasushi , Kawauchi Satoko , Ohkura Tsuyako , Iwaya Keiichi , Tsuda Hitoshi , Saitoh Daizoh , Sato Shunichi , Iwai Toshiaki 
Published: October 2015

AbstractDiagnosis of burn depths is crucial to determine the treatment plan for severe burn patients. However, an objective method for burn depth assessment has yet to be established, although a commercial laser Doppler imaging (LDI) system is used limitedly. We previously proposed burn depth assessment based on photoacoustic imaging (PAI), in which thermoelastic waves originating from blood under the burned tissue are detected, and we showed the validity of the method by experiments using rat models with three different burn depths: superficial dermal burn, deep dermal burn and deep burn. On the basis of those results, we recently developed a real‐time PAI system for clinical burn diagnosis. Before starting a clinical trial, however, there is a need to reveal more detailed diagnostic characteristics, such as linearity and error, of the PAI system as well as to compare its characteristics with those of an LDI system. In this study, we prepared rat models with burns induced at six different temperatures from 70 to 98 °C, which showed a linear dependence of injury depth on the temperature. Using these models, we examined correlations of signals obtained by PAI and LDI with histologically determined injury depths and burn induction temperatures at 48 hours postburn. We found that the burn depths indicated by PAI were highly correlative with histologically determined injury depths (depths of viable vessels) as well as with burn induction temperatures. Perfusion values measured by LDI were less correlative with these parameters, especially for burns induced at higher temperatures, being attributable to the limited detectable depth for light involving a Doppler shift in tissue. In addition, the measurement errors in PAI were smaller than those in LDI. On the basis of these results, we will be able to start clinical studies using the present PAI system.
Proteolytic fragmentation of inositol 1,4,5‐trisphosphate receptors: a novel mechanism regulating channel activity?
Authors: Wang Liwei , Alzayady Kamil J. , Yule David I. 
Published: October 2015

AbstractInositol 1,4,5‐trisphosphate receptors (IP3Rs) are a family of ubiquitously expressed intracellular Ca2+ release channels. Regulation of channel activity by Ca2+, nucleotides, phosphorylation, protein binding partners and other cellular factors is thought to play a major role in defining the specific spatiotemporal characteristics of intracellular Ca2+ signals. These properties are, in turn, believed pivotal for the selective and specific physiological activation of Ca2+‐dependent effectors. IP3Rs are also substrates for the intracellular cysteine proteases, calpain and caspase. Cleavage of the IP3R has been proposed to play a role in apoptotic cell death by uncoupling regions important for IP3 binding from the channel domain, leaving an unregulated leaky Ca2+ pore. Contrary to this hypothesis, we demonstrate following proteolysis that N‐ and C‐termini of IP3R1 remain associated, presumably through non‐covalent interactions. Further, we show that complementary fragments of IP3R1 assemble into tetrameric structures and retain their ability to be regulated robustly by IP3. While peptide continuity is clearly not necessary for IP3‐gating of the channel, we propose that cleavage of the IP3R peptide chain may alter other important regulatory events to modulate channel activity. In this scenario, stimulation of the cleaved IP3R may support distinct spatiotemporal Ca2+ signals and activation of specific effectors. Notably, in many adaptive physiological events, the non‐apoptotic activities of caspase and calpain are demonstrated to be important, but the substrates of the proteases are poorly defined. We speculate that proteolytic fragmentation may represent a novel form of IP3R regulation, which plays a role in varied adaptive physiological processes.
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Essential role of carbonic anhydrase XII in secretory gland fluid and HCO3− secretion revealed by disease causing human mutation
Authors: Hong Jeong Hee , Muhammad Emad , Zheng Changyu , Hershkovitz Eli , Alkrinawi Soliman , Loewenthal Neta , Parvari Ruti , Muallem Shmuel 
Published: October 2015

Key points
Fluid and HCO3− secretion is essential for all epithelia; aberrant secretion is associated with several diseases.

Carbonic anhydrase XII (CA12) is the key carbonic anhydrase in epithelial fluid and HCO3− secretion and works by activating the ductal Cl−–HCO3− exchanger AE2.
Delivery of CA12 to salivary glands increases salivation in mice and of the human mutation CA12(E143K) markedly inhibits it.
The human mutation CA12(E143K) causes disease due to aberrant CA12 glycosylation, and misfolding resulting in loss of AE2 activity.
AbstractAberrant epithelial fluid and HCO3− secretion is associated with many diseases. The activity of HCO3− transporters depends of HCO3− availability that is determined by carbonic anhydrases (CAs). Which CAs are essential for epithelial function is unknown. CA12 stands out since the CA12(E143K) mutation causes salt wasting in sweat and dehydration in humans. Here, we report that expression of CA12 and of CA12(E143K) in mice salivary glands respectively increased and prominently inhibited ductal fluid secretion and salivation in vivo. CA12 markedly increases the activity and is the major HCO3− supplier of ductal Cl−–HCO3− exchanger AE2, but not of NBCe1‐B. The E143K mutation alters CA12 glycosylation at N28 and N80, resulting in retention of the basolateral CA12 in the ER. Knockdown of AE2 and of CA12 inhibited pancreatic and salivary gland ductal AE2 activity and fluid secretion. Accordingly, patients homozygous for the CA12(E143K) mutation have a dry mouth, dry tongue phenotype. These findings reveal an unsuspected prominent role of CA12 in epithelial function, explain the disease and call for caution in the use of CA12 inhibitors in cancer treatment.
Intrinsic muscle clock is necessary for musculoskeletal health
Authors: Schroder Elizabeth A. , Harfmann Brianna D. , Zhang Xiping , Srikuea Ratchakrit , England Jonathan H. , Hodge Brian A. , Wen Yuan , Riley Lance A. , Yu Qi , Christie Alexander , Smith Jeffrey D. , Seward Tanya , Wolf Horrell Erin M. , Mula Jyothi , Peterson Charlotte A. , Butterfield Timothy A. , Esser Karyn A. 
Published: October 2015

Key points
The endogenous molecular clock in skeletal muscle is necessary for maintenance of phenotype and function.
Loss of Bmal1 solely from adult skeletal muscle (iMSBmal1−/−) results in reductions in specific tension, increased oxidative fibre type and increased muscle fibrosis with no change in feeding or activity.
Disruption of the molecular clock in adult skeletal muscle is sufficient to induce changes in skeletal muscle similar to those seen in the Bmal1 knockout mouse (Bmal1−/−), a model of advanced ageing.
iMSBmal1−/− mice develop increased bone calcification and decreased joint collagen, which in combination with the functional changes in skeletal muscle results in altered gait.
This study uncovers a fundamental role for the skeletal muscle clock in musculoskeletal homeostasis with potential implications for ageing.
AbstractDisruption of circadian rhythms in humans and rodents has implicated a fundamental role for circadian rhythms in ageing and the development of many chronic diseases including diabetes, cardiovascular disease, depression and cancer. The molecular clock mechanism underlies circadian rhythms and is defined by a transcription–translation feedback loop with Bmal1 encoding a core molecular clock transcription factor. Germline Bmal1 knockout (Bmal1 KO) mice have a shortened lifespan, show features of advanced ageing and exhibit significant weakness with decreased maximum specific tension at the whole muscle and single fibre levels. We tested the role of the molecular clock in adult skeletal muscle by generating mice that allow for the inducible skeletal muscle‐specific deletion of Bmal1 (iMSBmal1). Here we show that disruption of the molecular clock, specifically in adult skeletal muscle, is associated with a muscle phenotype including reductions in specific tension, increased oxidative fibre type, and increased muscle fibrosis similar to that seen in the Bmal1 KO mouse. Remarkably, the phenotype observed in the iMSBmal1−/− mice was not limited to changes in muscle. Similar to the germline Bmal1 KO mice, we observed significant bone and cartilage changes throughout the body suggesting a role for the skeletal muscle molecular clock in both the skeletal muscle niche and the systemic milieu. This emerging area of circadian rhythms and the molecular clock in skeletal muscle holds the potential to provide significant insight into intrinsic mechanisms of the maintenance of muscle quality and function as well as identifying a novel crosstalk between skeletal muscle, cartilage and bone.
The framed Standard Model (I) — A physics case for framing the Yang–Mills theory?
Authors: Chan Hong-Mo , Tsou Sheung Tsun 
Published: October 2015

Introducing, in the underlying gauge theory of the Standard Model, the frame vectors in internal space as field variables (framons), in addition to the usual gauge boson and matter fermions fields, one obtains: the standard Higgs scalar as the framon in the electroweak sector; a global [Formula: see text] symmetry dual to colour to play the role of fermion generations. Renormalization via framon loops changes the orientation in generation space of the vacuum, hence also of the mass matrices of leptons and quarks, thus making them rotate with changing scale [Formula: see text]. From previous work, it is known already that a rotating mass matrix will lead automatically to: CKM mixing and neutrino oscillations, hierarchical masses for quarks and leptons, a solution to the strong-CP problem transforming the theta-angle into a Kobayashi–Maskawa phase. Here in the framed standard model (FSM), the renormalization group equation has some special properties which explain the main qualitative features seen in experiment both for mixing matrices of quarks and leptons, and for their mass spectrum. Quantitative results will be given in Paper II. The present paper ends with some tentative predictions on Higgs decay, and with some speculations on the origin of dark matter.
Preclinical Evidence That Trametinib Enhances the Response to Antiangiogenic Tyrosine Kinase Inhibitors in Renal Cell Carcinoma
Authors: Bridgeman Victoria L. , Wan Elaine , Foo Shane , Nathan Mark R. , Welti Jonathan C. , Frentzas Sophia , Vermeulen Peter B. , Preece Natasha , Springer Caroline J. , Powles Thomas , Nathan Paul D. , Larkin James , Gore Martin , Vasudev Naveen S. , Reynolds Andrew R. 
Published: October 2015

AbstractSunitinib and pazopanib are antiangiogenic tyrosine kinase inhibitors (TKI) used to treat metastatic renal cell carcinoma (RCC). However, the ability of these drugs to extend progression-free and overall survival in this patient population is limited by drug resistance. It is possible that treatment outcomes in RCC patients could be improved by rationally combining TKIs with other agents. Here, we address whether inhibition of the Ras-Raf-MEK-ERK1/2 pathway is a rational means to improve the response to TKIs in RCC. Using a xenograft model of RCC, we found that tumors that are resistant to sunitinib have a significantly increased angiogenic response compared with tumors that are sensitive to sunitinib in vivo. We also observed significantly increased levels of phosphorylated ERK1/2 in the vasculature of resistant tumors, when compared with sensitive tumors. These data suggested that the Ras-Raf-MEK-ERK1/2 pathway, an important driver of angiogenesis in endothelial cells, remains active in the vasculature of TKI-resistant tumors. Using an in vitro angiogenesis assay, we identified that the MEK inhibitor (MEKI) trametinib has potent antiangiogenic activity. We then show that, when trametinib is combined with a TKI in vivo, more effective suppression of tumor growth and tumor angiogenesis is achieved than when either drug is utilized alone. In conclusion, we provide preclinical evidence that combining a TKI, such as sunitinib or pazopanib, with a MEKI, such as trametinib, is a rational and efficacious treatment regimen for RCC. Mol Cancer Ther; 15(1); 172–83. ©2015 AACR.