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Despite the wide range of studies on how students’ past knowledge influences their understanding of scientific terminology, few studies were conducted to compare non-scientific language with scientific language, or rather everyday language with scientific language, from a cognitive linguistic perspective. The present paper aims to determine the cognitive mechanisms, i.e., image schemas, conceptual metaphor, and conceptual metonymy, which underpin the conceptualisation of the Arabic term سرعة (speed), using a conceptual metaphor theory framework. Thus, the research question guiding this study is: What cognitive mechanisms underlie the concept of سرعة (speed) in Arabic? The findings of this study will shed light on how Arab speakers conceptualise this term, demonstrating their background knowledge of the term compared to its scientific meaning. The article adds to the growing body of cognitive linguistics research on the conceptual processes behind physics terms. The data was collected from the Arabic Web Corpus (arTenTen) using the Sketch Engine. The findings demonstrated that VERTICATLITY and SCALE schemas are the most dominant image schemas that anchor the conceptual meaning in Arab speakers’ perceptions of the term under investigation and the discourse in which it is employed, as well as offer the concrete basis for conceptual metaphors. The conceptual metaphor CHANGE IS MOTION (LOCATION) was also shown to be active in motivating the conception of SPEED in Arabic.

PDF file - 383K, Tumors from homozygous ErbB3delta85/delta85 show a typical ErbB2/Neu histological pattern

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PDF file - 31K, SacI- and SpeI/SphI-digested genomic DNA from mice with the indicated genotypes

PDF file - 209K, Proliferative capacity and apoptotic status of ErbB3delta85/delta85/NDL2-5 mammary tumors

The formation of ErbB2/ErbB3 heterodimers plays a critical role in ErbB2-mediated signaling in both normal mammary development and mammary tumor progression. Through 7 phosphoinositide 3-kinase (PI3K) phosphotyrosine-binding sites, ErbB3 is able to recruit PI3K and initiate the PI3K/AKT signaling pathway. To directly explore the importance of the ErbB3/PI3K pathway in mammary development and tumorigenesis, we generated a mouse model that carries a mutant ErbB3 allele lacking the seven known PI3K-binding sites (ErbB3Δ85). Mice homozygous for the ErbB3Δ85 allele exhibited an initial early growth defect and a dramatic impairment of mammary epithelial outgrowth. Although homozygous adult mice eventually recovered from the growth defect, their mammary glands continued to manifest the mammary outgrowth and lactation defects throughout their adult life. Interestingly, despite the presence of a profound mammary gland defect, all of the female ErbB3Δ85 mice developed metastatic ErbB2-induced mammary tumors secondary to mammary epithelial expression of an activated ErbB2 oncogene capable of compensatory PI3K signaling from both EGF receptor and ErbB2. Our findings therefore indicate that, although ErbB3-associated PI3K activity is critical for mammary development, it is dispensable for ErbB2-induced mammary tumor progression. Cancer Res; 72(12); 3080–90. ©2012 AACR.

PDF file - 54K, Progeny of ErbB3D85 breeding pairs

PDF file - 356K, Activation status of Shc, Src and members of the PI-3K signaling pathway

PDF file - 47K, Metastatic capacity of ErbB3delta85/delta85/NDL2-5 mammary tumors

Despite the considerable number of studies on vocabulary and sense relations such as polysemy, they are confined to comparing vocabulary learning methods and strategies and examining the usefulness of certain sense relations in acquiring L2 vocabulary. Until now, no attempt has been made to analyse polysemy in English textbooks used in non-native English contexts. The aim of the current article was to explore the high usage of the most frequently used words from the selected English textbooks in real-life English and to determine the extent to which polysemy is incorporated in the selected English textbooks. The data was collected from two textbooks: _Close-up_ (Intermediate Secondary) and _Full Blast Plus 4_ (Upper Secondary). The _Sketch Engine_ word list tool was used to determine the top 100 most frequently used words in the first sub-corpus, _Close-up_ (Intermediate Secondary), and the top 100 most frequently used words in the second sub-corpus, _Full Blast Plus 4_ (Upper Secondary). The use of the chosen words in the _British National Corpus_ (BNC) was explored using the _Sketch Engine_ to determine whether they are the most commonly used in English. _WordNet_ was also used to determine the polysemy and frequency of the words under study. The findings revealed the top 100 most frequently used words in _Close-up_ and _Full Blast Plus 4_ have high frequency levels (ranks) in the _BNC_, yet 65 of the top 100 most frequently used words in both Close-up and Full Blast Plus 4 overlapped despite the level difference. Furthermore, polysemy is only lightly emphasised in the textbooks concerned. The results of the present study have important implications for second and foreign language learning research and education.

The current paper investigates two productive morphological processes, namely compounds and portmanteau words (or blends). While compounds, a productive, regular and predicable morphological process, have received much attention in the literature, little attention was paid to portmanteau words, a creative, irregular and unpredictable word formation process. The present paper aims to find the commonalities and differences between these morphological devices, using Rosch et al.’s (1975; 1976) theory of prototypes and basic-level categories to achieve this goal. This theory will also be employed to discuss the literature on the word formation mechanisms under investigation and propose a new categorization approach to these neologisms. The analysis suggests that compounds and blends compare and contrast and that the distinctions between them are blurry. The analysis confirms that a prototypical approach is well suited to compounds and blends in English. This has implications for future research into English word-formation processes in general and compounds and blends precisely.

Conceptual metaphors have received much attention in research on discourse about infectious diseases in recent years. Most studies found that conceptual metaphors of war dominate media discourse about disease. Similarly, a great deal of research has been undertaken on the new coronavirus, i.e., COVID-19, especially in the English news discourse as opposed to other languages. The present study, in contrast, analyses the conceptual metaphors used in COVID-19 discourse in French-language newspapers. The study explored the linguistic metaphors used in COVID-19 discourse in these newspapers and conceptual metaphors that underlie and motivate them, using a conceptual metaphor theory framework (CMT). Therefore, two North African French-language newspapers, namely Libération, published in Morocco, and La Presse de Tunisie, published in Tunisia, formed the corpus of the current study. The results showed that the most frequent framing of COVID-19 was in terms of WAR, followed by DISASTER and KILLER, respectively.

The current paper expands on previous work done on the influence of learners’ language and pre-existing knowledge on understanding physics terminology by exploring the concept of ACCELERATION in Arabic and English. The study attempts to answer two questions: (1) what are the similarities and differences between the polysemy of Arabic تسارع (tasāruʿ) (acceleration) and the polysemy of English acceleration, and (2) to what extent do prototypes and factors motivating the conceptualization of تسارع (tasāruʿ) and the conceptualization of acceleration converge or diverge? To this end, Arabic and English dictionaries and corpora, the ArabiCorpus (Arabic Corpus Search Tool) and the British National Corpus (BNC), were employed. The dictionaries were surveyed to explore the various meanings of تسارع (tasāruʿ) and acceleration, while the ArabiCorpus and the BNC were employed to investigate the senses and to identify the most frequent collocates and so the prototypes of these terms. The meaning extension of the terms is examined on the basis of the cognitive mechanisms which appear in the corpora. Theoretically, the paper is informed by the prototype theory (Rosch, 1973; 1975), image schemas (Johnson, 1987), and conceptual metaphor (Lakoff & Johnson, 1980/2003). The results show that تسارع (tasāruʿ) (acceleration) and acceleration generally overlap in terms of polysemy, prototype, and images schemas as well as conceptual metaphor that organize the conceptualization of these terms. It was also found that both Arab and English speakers mix ACCELERATION up with SPEED and so misunderstand them in a scientific setting. The present findings have several implications for science curriculum design, education, and research on universal and culture-specific properties of language.

The present paper aims to broaden the current understanding of students’ misconception of scientific terminology by identifying the gaps between Arabic and English scientific terminologies and between everyday language and scientific language. The paper compares the polysemy, prototypes, and motivating factors of English energy with those of Arabic طاقة (ṭāqa), with more focus on students’ prior knowledge. The study employs Lakoff’s (1987) idealized cognitive models and Rosch’s (1975) prototype theory to reveal the radial members of both categories, i.e., energy and طاقة (ṭāqa), and to explain the kinds of cognitive mechanisms that motivate the extension as well as understanding of the meanings of these terms. To this end, the study uses several English and Arabic dictionaries, lexical databases and corpora. This is to explore all the meanings, prototypes and motivating factors of the terms under investigation. The results show that the terms energy and طاقة (ṭāqa) overlap in prototypical meanings and motivating factors but differ in less prototypical and peripheral meanings. English and Arabic learners may then face similar issues in learning scientific concepts due to the difference between their pre-existing knowledge and scientific language.

The present article analyses the semantic structure of the colour term (green) in Arabic to establish whether it has undergone a change in terms of meanings and prototypes and to identify the motivating factors for its semantic change. The current study compares and contrasts the polysemy of (green) in premodern texts and modern texts. To explore the meanings of the word and to identify its most frequent collocates and thus most prototypical meanings, the study employs the ArabiCorpus (Arabic Corpus Search Tool). The data collected on the term are analysed in accordance with Rosch’s [1] [2] prototype theory, and Lakoff and Johnson’s [3] conceptual metonymy and conceptual metaphor. The results show that scores highly in its average occurrence in both premodern texts and modern texts and maintains its favourable meaning despite the variance in its prototypical meanings across the selected subcorpora. Its semantic expansion is motivated by conceptual metonymy, conceptual metaphor and loan translation respectively.

The formation of ErbB2/ErbB3 heterodimers plays a critical role in ErbB2-mediated signaling in both normal mammary development and mammary tumor progression. Through 7 phosphoinositide 3-kinase (PI3K) phosphotyrosine-binding sites, ErbB3 is able to recruit PI3K and initiate the PI3K/AKT signaling pathway. To directly explore the importance of the ErbB3/PI3K pathway in mammary development and tumorigenesis, we generated a mouse model that carries a mutant ErbB3 allele lacking the seven known PI3K-binding sites (ErbB3Δ85). Mice homozygous for the ErbB3Δ85 allele exhibited an initial early growth defect and a dramatic impairment of mammary epithelial outgrowth. Although homozygous adult mice eventually recovered from the growth defect, their mammary glands continued to manifest the mammary outgrowth and lactation defects throughout their adult life. Interestingly, despite the presence of a profound mammary gland defect, all of the female ErbB3Δ85 mice developed metastatic ErbB2-induced mammary tumors secondary to mammary epithelial expression of an activated ErbB2 oncogene capable of compensatory PI3K signaling from both EGF receptor and ErbB2. Our findings therefore indicate that, although ErbB3-associated PI3K activity is critical for mammary development, it is dispensable for ErbB2-induced mammary tumor progression. Cancer Res; 72(12); 3080–90. ©2012 AACR.

Iris is a software architecture for building highly reconfigurable radio networks. It has formed the basis for a wide range of dynamic spectrum access and cognitive radio demonstration systems presented at a number of international conferences between 2007 and 2010. These systems have been developed using heterogeneous processing platforms including general-purpose processors, field-programmable gate arrays and the Cell Broadband Engine. Focusing on runtime reconfiguration, Iris offers support for all layers of the network stack and provides a platform for the development of not only reconfigurable point-to-point radio links but complete networks of cognitive radios. This article provides an overview of Iris, presenting the unique features of the architecture and illustrating how it can be used to develop a cognitive radio testbed.

Somatostatin is a neuropeptide that acts as an endogenous inhibitor of various cellular functions including endocrine and exocrine secretions and the proliferation of normal and tumour cells. Its action is mediated by a family of G-protein-coupled receptors (sst1–sst5) that are widely distributed in normal and tumour cells. Gastroenteropancreatic endocrine tumours express multiple somatostatin receptors, sst2 being clearly predominant. These receptors represent the molecular basis for the clinical use of somatostatin analogues in the treatment of endocrine tumours and their in vivo localisation. This review covers current knowledge in somatostatin receptor biology and signalling.

Somatostatin is a neuropeptide family that is produced by neuroendocrine, inflammatory, and immune cells in response to different stimuli. Somatostatin acts as an endogenous inhibitory regulator of various cellular functions including secretions, motility, and proliferation. Its action is mediated by a family of G-protein-coupled receptors (called sst1-sst5) that are widely distributed in the brain and periphery. The five receptors bind the natural peptides with high affinity, but only sst2, sst5, and sst3 bind the short synthetic analogs used to treat acromegaly and neuroendocrine tumors. This review covers the current knowledge in somatostatin receptor biology and signaling.

Somatostatin is an inhibitory neuropeptide, which acts on various targets throughout the body to regulate a variety of physiological functions including inhibition of endocrine and exocrine secretions, modulation of neurotransmission, motor and cognitive functions, inhibition of intestinal motility, absorption of nutrients and ions, vascular contractility and inhibition of normal and tumour cell proliferation. It exerts its effects through interaction with five somatostatin receptors (sst1–sst5), which belong to the family of G-protein-coupled receptors with seven transmembrane spanning domains and are variably expressed in a variety of tumours such as gastroenteropancreatic tumours, pituitary tumours, and carcinoid tumours. This review covers the present knowledge regarding the molecular mechanisms involved in somatostatin antineoplastic activity. Evidence that sst2 receptor acts as a tumour suppressor is also discussed.

The G protein-coupled sst2 somatostatin receptor is a critical negative regulator of cell proliferation. sstII prevents growth factor-induced cell proliferation through activation of the tyrosine phosphatase SHP-1 leading to induction of the cyclin-dependent kinase inhibitor p27Kip1. Here, we investigate the signaling molecules linking sst2 to p27Kip1. In Chinese hamster ovary-DG-44 cells stably expressing sst2 (CHO/sst2), the somatostatin analogue RC-160 transiently stimulates ERK2 activity and potentiates insulin-stimulated ERK2 activity. RC-160 also stimulates ERK2 activity in pancreatic acini isolated from normal mice, which endogenously express sst2, but has no effect in pancreatic acini derived from sst2 knock-out mice. RC-160-induced p27Kip1 up-regulation and inhibition of insulin-dependent cell proliferation are both prevented by pretreatment of CHO/sst2 cells with the MEK1/2 inhibitor PD98059. In addition, using dominant negative mutants, we show that sst2-mediated ERK2 stimulation is dependent on the pertussis toxin-sensitive Gi/o protein, the tyrosine kinase Src, both small G proteins Ras and Rap1, and the MEK kinase B-Raf but is independent of Raf-1. Phosphatidylinositol 3-kinase (PI3K) and both tyrosine phosphatases, SHP-1 and SHP-2, are required upstream of Ras and Rap1. Taken together, our results identify a novel mechanism whereby a Gi/o protein-coupled receptor inhibits cell proliferation by stimulating ERK signaling via a SHP-1-SHP-2-PI3K/Ras-Rap1/B-Raf/MEK pathway.

We report here that apelin (65–77) induces activation of extracellular-regulated kinases (ERKs) in Chinese hamster ovary (CHO) cells expressing the msr/apj receptor. This concentration-dependent activation was transient, peaking at 5 min. Pretreatment of CHO cells with pertussis toxin fully abrogated ERK phosphorylation, whereas overexpression of the β-adrenergic receptor kinase-1 C-terminal fragment did not alter ERK activation. Transfection with a dominant-negative mutant of Ras was without effect on ERK activation, whereas an inhibitor of many protein kinase C isoforms, GF109203X, strongly decreased it. These results demonstrate that stimulation of the murine msr/apj receptor promotes ERK activation via the α subunit of a pertussis toxin-sensitive protein in a Ras-independent pathway.

In mice pretreated intracerebroventricularly (i.c.v.) with pertussis or cholera toxins, effects of neuropeptide FF (NPFF), on hypothermia and morphine-induced analgesia, were assessed. NPFF and a potent NPFF agonist, 1DMe (0.005–22 nmol) injected into the lateral ventricle decreased morphine analgesia and produced naloxone (2.5 mg kg −1 , s.c.)-resistant hypothermia after administration into the third ventricle. Cholera toxin (CTX 1 μg, i.c.v.) pretreatment (24 or 96 h before) inhibited the effect of 1DMe on body temperature, but failed to reverse its anti-opioid activity in the tail-flick test. CTX reduced hypothermia induced by a high dose of morphine (8 nmol, i.c.v.) but not the analgesic effect due to 3 nmol morphine. Pertussis toxin (PTX) pretreatment inhibited both morphine-hypothermia and -analgesia but did not modify hypothermia induced by 1DMe. The present results suggest that NPFF-induced hypothermia depends on the stimulation of Gs (but not Gi) proteins. In contrast, anti-opioid effects resulting from NPFF-receptor stimulation do not involve a cholera toxin-sensitive transducer protein.

This paper describes the acceleration of a MonteCarlo algorithm for pricing a LIBOR swaption portfolio using multi-core CPUs and GPUs. Speedups of up to 305x are achieved on two Nvidia Tesla M2050 GPUs and up to 20.8x on two Intel Xeon E5620 CPUs, compared to a sequential CPU implementation. This performance is achieved by using the Xcelerit platform - writing sequential, high-level C++ code and adopting a simple dataflow programming model. It avoids the complexity involved when using low-level high-performance computing frameworks such as OpenMP, OpenCL, CUDA, or SIMD intrinsics. The paper provides an overview of the Xcelerit platform, details how high performance is achieved through various automatic optimisation and parallelisation techniques, and shows how the tool can be used to implement portable accelerated Monte-Carlo algorithms in finance. It illustrates the implementation of the Monte-Carlo LIBOR swaption portfolio pricer and gives performance results. A comparison of the Xcelerit platform implementation with an equivalent low-level CUDA version shows that the overhead introduced is less than 1.5% in all scenarios.

Introduction: Activation of focal adhesion kinase (FAK) is hypothesized to play an important role in the pathogenesis of human breast cancer.Methods: To directly evaluate the role of FAK in mammary tumour progression, we have used a conditional FAK mouse model and mouse mammary tumour virus (MMTV)-driven Cre recombinase strain to inactivate FAK in the mammary epithelium of a transgenic mouse model of ErbB2 breast cancer.Results: Although mammary epithelial disruption of FAK in this model resulted in both a delay in onset and a decrease in the number of neoplastic lesions, mammary tumours occurred in 100% of virgin female mice. All of the tumours and derived metastases that developed were proficient for FAK due to the absence of Cre recombinase expression. The hyperplastic epithelia where Cre-mediated recombination of FAK could be detected exhibited a profound proliferative defect. Consistent with these observations, disruption of FAK in established tumour cells resulted in reduced tumour growth that was associated with impaired proliferation. To avoid the selection for FAK-proficient ErbB2 tumour epithelia through escape of Cre-mediated recombination, we next intercrossed the FAK conditional mice with a separate MMTV-driven ErbB2 strain that co-expressed ErbB2 and Cre recombinase on the same transcriptional unit.Conclusions: While a delay in tumour induction was noted, FAK-deficient tumours arose in 100% of female animals indicating that FAK is dispensable for ErbB2 tumour initiation. In addition, the FAK-null ErbB2 tumours retained their metastatic potential. We further demonstrated that the FAK-related Pyk2 kinase is still expressed in these tumours and is associated with its downstream regulator p130Cas. These observations indicate that Pyk2 can functionally substitute for FAK in ErbB2 mammary tumour progression.

Consistent with their essential role in cell adhesion to the extracellular matrix, integrins and their associated signaling pathways have been shown to be involved in cell proliferation, migration, invasion and survival, processes required in both tumorigenesis and metastasis. β1-integrins represent the predominantly expressed integrins in mammary epithelial cells and have been proven crucial for mammary gland development and differentiation. Here we provide an overview of the studies that have used transgenic mouse models of mammary tumorigenesis to establish β1-integrin as a critical mediator of breast cancer progression and thereby as a potential therapeutic target for the development of new anticancer strategies.

The focus of this paper is an experimentation platform known as Iris that has a runtime reconfigurable software radio at its core. We have employed this platform to enable a wide variety of tests and experimentation in the fields of dynamic spectrum access and cognitive radio. The paper charts the progress of the Iris system since its inception as well as details of some of the experiments and trials conducted using this platform. We also discuss the challenges involved in the development and deployment of a software radio platform that supports runtime reconfigurability and provide recommendations for future improvements.

Elevated expression and activation of the focal adhesion kinase (FAK) occurs in a large proportion of human breast cancers. Although several studies have implicated FAK as an important signaling molecule in cell culture systems, evidence supporting a role for FAK in mammary tumor progression is lacking. To directly assess the role of FAK in this process, we have used the Cre/loxP recombination system to disrupt FAK function in the mammary epithelium of a transgenic model of breast cancer. Using this approach, we demonstrate that FAK expression is required for the transition of premalignant hyperplasias to carcinomas and their subsequent metastases. This dramatic block in tumor progression was further correlated with impaired mammary epithelial proliferation. These observations provide direct evidence that FAK plays a critical role in mammary tumor progression.

Many studies have implicated tyrosine phosphatases in the down-regulation of growth factor signaling pathways. It is becoming evident that some of them, including SHP-1, SHP-2 and PTPη, have a role in SSTR signaling. However, there are many issues which remain to be clarified. These include the identification of SST-mediated pathways in which these PTPs participate, as well as their physiological substrates and binding partners and the precise molecular mechanisms, which permit their interaction with sst receptors and/or associated molecules. In addition, the respective role of these PTP for each receptor subtype pathway awaits further study. Genetic approaches including gene targeting, RNA interference (RNAi) and new technologies including proteomic analysis and cell imaging for the detection and analysis of signalling complexes, will provide powerful tools to elucidate these important questions.

Somatostatin is a neuropeptide that acts as an endogenous inhibitor of various cellular functions including endocrine and exocrine secretions and the proliferation of normal and tumour cells. Its action is mediated by a family of G-protein-coupled receptors (sst1-sst5) that are widely distributed in normal and tumour cells. Gastroenteropancreatic endocrine tumours express multiple somatostatin receptors, sst2 being clearly predominant. These receptors represent the molecular basis for the clinical use of somatostatin analogues in the treatment of endocrine tumours and their in vivo localisation. This review covers current knowledge in somatostatin receptor biology and signalling.

Gap junctions are composed of connexins and are critical for the maintenance of the differentiated state. Consistently, connexin expression is impaired in most cancer cells, and forced expression of connexins following cDNA transfection reverses the tumor phenotype. We have found that the restoration of density inhibition of human pancreatic cancer cells by the antiproliferative somatostatin receptor 2 (sst2) is due to overexpression of endogenous connexins Cx26 and Cx43 and consequent formation of functional gap junctions. Immunoblotting along with protein metabolic labeling and mRNA monitoring revealed that connexin expression is enhanced at the level of translation but is not sensitive to the inhibition of cap-dependent translation initiation. Furthermore, we identified a new internal ribosome entry site (IRES) in the Cx26 mRNA. The activity of Cx26 IRES and that of the previously described Cx43 IRES are enhanced in density-inhibited cells. These data indicate that the restoration of functional gap junctions is likely a critical event in the antiproliferative action of the sst2 receptor. We further suggest that the existence of IRESes in connexin mRNAs permits connexin expression in density-inhibited or differentiated cells, where cap-dependent translation is generally reduced.