The Building Blocks of Child Bilingual Code-Mixing: A Cross-Corpus Traceback Approach

This paper offers an inductive, exploratory study on the role of input and individual differences in the early code-mixing of bilingual children. Drawing on data from two German-English bilingual children, aged 2–4, we use the traceback method to check whether their code-mixed utterances can be accounted for with the help of constructional patterns that can be found in their monolingual data and/or in their caregivers’ input. In addition, we apply the tracebackmethod to checkwhether the patterns used by one child can also be found in the input of the other child. Results show that patterns found in the code-mixed utterances could be traced back to the input the children receive, suggesting that children extract lexical knowledge from their environment. Additionally, tracing back patterns within each child was more successful than tracing back to the other child’s corpus, indicating that each child has their own set of patterns which depends verymuch on their individual input. As such, these findings can shed new light on the interplay of the two developing grammars in bilingual children and their individual differences

Effects of progesterone on hyperoxia-induced damage in mouse C8-D1A astrocytes

Introduction The birth of most mammals features a dramatic increase in oxygen while placenta-derived hormones such as β-estradiol and progesterone plummet. In experimental newborn animals, transiently elevated oxygen concentrations cause death of neurons, astrocytes, and oligodendrocyte precursors. High oxygen has been associated with cerebral palsy in human preterm infants while progesterone is being used to prevent preterm delivery and investigated as a neuroprotective agent. Methods In this study, we investigated the effects of hyperoxia (80% O2 for 24, 48, and 72 h) on cultured C8-D1A astrocytes in the presence or absence of progesterone at concentrations ranging from 10−9 to 10−5 mol/L. Results Hyperoxia measured by methytetrazolium assay (MTT) reduced cell viability, increased release of lactate dehydrogenase (LDH), reduced carboxyfluorescein diacetate succinimidyl ester (CFSE)-assessed cell proliferation, and downregulated Cylin D2 expression. Progesterone did not affect any of these hyperoxia-mediated indicators of cell death or malfunctioning. Real-time PCR analysis showed that hyperoxia caused downregulation of the progesterone receptors PR-AB und PR-B. Conclusions Our experiments showed that there was no protective effect of progesterone on hyperoxia-inducted cell damage on mouse C8-D1A astrocytes. Down regulation of the progesterone receptors might be linked to the lack of protective effects

The Traceback method in child language acquisition research: Identifying patterns in early speech

This paper discusses the traceback method, which has been the basis of some influential papers on first language acquisition. The method sets out to demonstrate that many or even all utterances in a test corpus (usually the last two sessions of recording) can be accounted for with the help of recurrent fixed strings (like What’s that?) or frame-and-slot patterns (like [What’s X?]) that can also be identified in the remaining dataset (i.e., the previous sessions of recording). This is taken as evidence that language learning is much more item-based than previously assumed. In the present paper we sketch the development of the method over the last two decades, and discuss its relation to usage-based theory, as well as the cognitive plausibility of its components, and we highlight both its potential and its limitations

Priming of Frames and Slots in Bilingual Children’s Code-Mixing: A Usage-Based Approach

This article investigates the role of direct input in the code-mixing of three bilingual children aged 2–4 years acquiring English as one language, and either German, Polish, or Finnish as the other. From a usage-based perspective, it is assumed that early children’s utterances are item-based and that they contain many lexically fixed patterns. To account for such patterns, the traceback method has been developed to test the hypothesis that children’s utterances are constructed on the basis of a limited inventory of chunks and frame-and-slot patterns. We apply this method to the code-mixed utterances, suggesting that much of the code-mixing occurs within frame-and-slot patterns, such as Was ist X? as in Was ist breakfast muesli? “What is breakfast muesli?” We further analyzed each code-mixed utterance in terms of priming. Our findings suggest that much of the early code-mixing is based on concrete lexically fixed patterns which are subject to input occurring in immediately prior speech, either the child’s own or that of her caregivers

Protektive Strategien im Hyperoxie-Schädigungsmodell der neonatalen Ratte

Die Frühgeburtlichkeit ist ein weltweites Problem und betrifft etwa 10-20% der neugeborenen Kinder und ist die häufigste Todesursache bei Kindern unter 5 Jahren. In Deutschland kommt etwa jedes zehnte Kind zu früh auf die Welt, davon etwa 12% mit einem Geburtsgewicht unter 1500 g. Ein geringes Geburtsgewicht und postnatale Komplikationen korrelieren dabei mit einem erhöhten Risiko für Mortalität und Morbidität. Präventive und therapeutische Interventionen haben in den letzten Jahrzehnten die Überlebensrate verbessert, jedoch ist weiterhin insbesondere bei Kindern mit einem Geburtsgewicht unter 1500 g eine hohe Morbiditätsrate zu beklagen. Abgesehen von der systemischen und organischen Unreife des zu früh geborenen Kindes, gibt es eine Vielzahl an exogenen Noxen, die in der Pathogenese frühgeburtlicher Erkrankungen eine Rolle spielen können. Neben der Sauerstofftoxizität, resultierend aus den unphysiologisch hohen Sauerstoffkonzentrationen, denen Frühgeborene aufgrund der Geburt und notwendiger Sauerstoffsupplementierung ausgesetzt sind, sind medikamentöse Insulte, wie Anästhetika, als ebenso kausal anzusehen. Die Unreife bedingt dabei ein Ungleichgewicht physiologischer Prozesse, wie des respiratorischen Systems und des anti-oxidativen Abwehrsysteme. In dieser redox-instabilen Situation können zahlreiche medizinisch notwendige medikamentöse oder therapeutische Insulte modulierend wirken und sind mit Nebenwirkungen für die Kurz- und Langzeitentwicklung behaftet. Oxidativer Stress spielt bei der Pathogenese vieler Erkrankungen der Frühgeborenen eine entscheidende Rolle, wobei die kausalen Pathologien bisher unvollständig verstanden sind. Neben der Klärung der pathologischen Prozesse, ist die Identifizierung möglicher therapeutischer Strategien Ziel der neonatologischen Forschung. Klinische Studien belegen bereits die protektive Wirkung von Koffein, einem in der Neonatologie eingesetztem Medikament zur Behandlung und Prävention von Frühgeborenen-Apnoen, für das Langzeit-Outcome von Frühgeborenen und auch die möglichen neuroprotektiven Effekte von Dexmedetomidin, einem Sedativa mit vielseitigen pharmakologischen Wirkungen, da aber subtile Störungen der neurologischen Entwicklung im Umfeld von Frühgeburtlichkeit, neonatalen Adaptationsstörungen und intensivmedizinische Maßnahmen Einfluss nehmen können, können standardisierte Tierversuche dazu beitragen, potentiell protektive Effekte von Koffein und Dexmedetomidin im sich entwickelnden Gehirn und/oder der unreifen Lunge zu identifizieren. Dazu wurden Untersuchungen der infantilen Ratte, einem neonatalen entwicklungsadäquaten Tiermodell, in einem akuten Hyperoxie-Schädigungsmodell durchgeführt. Ziel der Untersuchungen war, ob die Präkonditionierung mit Koffein oder Dexmedetomidin unter postnataler, akuter Hyperoxie (6, 24 und/oder 48 Stunden), die durch oxidativen Stress assoziierten, zellulären Veränderungen reduzieren kann. Oxidativer Stress im akuten Sauerstoffschädigungsmodell im unreifen Gehirn der Ratte beeinträchtigte die hippocampale Neurogenese und induzierte die oxidativen Stress-Kaskade mit daraus resultierender Neuroinflammation und Neurodegeneration. Des Weiteren scheint die anti-oxidative Abwehrkapazität während der Exposition gegenüber Hyperoxie vermindert zu sein. Eine Präkonditionierung mit einer Einzeldosis Koffein (10 mg/kg KGW) vor dem hyperoxischem Insult verringerte die durch oxidativen Stress ausgelöste Neuroinflammation und Neurodegeneration und verstärkte die anti-oxidative Stressantwort. Anti-inflammatorische Effekte zeigte Koffein auch in der unreifen Lunge mit einer adäquaten Inhibierung der Immunzellinfiltration, einer Reduktion der pro-inflammtorischen Antwort und Verminderung der Chemokin-Expression. Neben der unselektiven Antagonisierung der Adenosinrezeptoren, scheint Koffein per se anti-oxidative Eigenschaften zu vermitteln. Das zur Präkonditionierung eingesetzte Dexmedetomidin (1, 5 und 10 µg/kg KGW) zeigte neuroprotektive Eigenschaften in unserem Modell der oxidativen Stress-Schädigung im sich entwickelnden Rattenhirn, wobei apoptotischer Zelltod und pro-inflammatorische Zytokininsulte inhibiert und die postnatale Neurogenese und neuronale Plastizität erhalten wurden. Dexmedetomidin erhöhte die Proliferationskapazität von mitotischen Zellen, was letztlich zu höheren Zellzahlen von reifen Neuronen führte, ohne die Apoptoserate bei Kontrolltieren zu beeinflussen. Die anti-oxidativen und anti-inflammatorischen Eigenschaften von Dexmedetomidin über die 2-Adrenorezeptor-Agonisierung scheint eine potente Möglichkeit der Neuroprotektion darzustellen. Weiterführende Untersuchungen zu protektiven Medikamenten mit anti-oxidativen Eigenschaften, die bereits in der neonatalen Intensivversorgung als Medikament zugelassen sind, sollten weiterhin im Fokus klinischer und experimenteller Studien stehen, um pharmakokinetische und molekulare Mechanismen besser verstehen zu können und die Effektivität und Sicherheit beim klinischen Einsatz zu erhöhen, um nicht-vermeidbare medizinisch-induzierte Maßnahmen mit einem verbessertem Outcome für frühgeborene Kinder in Einklang zu bringen.Preterm birth is a global problem affecting about 10-20% of newborn children and is the leading cause of death in children under the age of 5 years. In Germany, about one child in ten is born prematurely, of which about 12% have a birth weight of less than 1500 g. Low birth weight and postnatal complications correlate with an increased risk of mortality and morbidity. Preventive and therapeutic interventions have improved survival in recent decades, but are still associated with high morbidity rates, especially in infants with a birth weight below 1500 g. Apart from the systemic and organic immaturity of the prematurely infants, there are a variety of exogenous insults that may play a role in the pathogenesis of prematurity. In addition to the oxygen toxicity resulting from the unphysiological high oxygen concentrations to which premature infants are exposed as a result of birth and the need for oxygen supplementation, medical insults such as anesthetics are also considered causal. Immaturity causes an imbalance of physiological processes, such as the respiratory system and the anti-oxidative defense systems. In this redox-unstable situation, numerous medically necessary medical or therapeutic insults can have a modulating effect and are associated with side effects for short and long term development. Oxidative stress plays a crucial role in the pathogenesis of many premature infant diseases, but causes underlying are incompletely understood. In addition to the clarification of pathological processes, the identification of possible therapeutic strategies is the goal of neonatological research. Clinical trials are already demonstrating the protective effects of caffeine, a neonatal drug for the treatment and prevention of apnea of prematurity, for the long term outcome of preterm infants and the potential neuroprotective effects of dexmedetomidine, a sedative with versatile pharmacological effects. Standardized animal studies may help to identify potential protective effects of caffeine and dexmedetomidine in the developing brain and / or immature lung, as subtle neurodevelopmental disorders may be influenced by premature birth, neonatal adaptation disorders and critical care settings. For this purpose, studies in neonatal rats were designed using an acute model of hyperoxia damage. The aim of the study was to determine whether preconditioning with caffeine or dexmedetomidine under postnatal hyperoxia (6, 24, and/or 48 hours) may reduce cellular changes associated with oxidative stress. As a major result in the immature rat brain, hippocampal neurogenesis was affected and the oxidative stress cascade was induced by hyperoxia, hence resulting in neuroinflammation and neurodegeneration. Furthermore, anti-oxidative defense capacity during exposure to hyperoxia appears to be diminished. Pre-conditioning with a single dose of caffeine (10 mg/kg bodyweight) prior to the hyperoxic insult reduced neuroinflammation and neurodegeneration caused by hyperoxia, and it enhanced the anti-oxidative stress response. Caffeine also revealed anti-inflammatory properties in the immature lung with strong inhibition of immune cell infiltration, inhibition of the pro-inflammatory response, and reduction in chemokine expression. In addition to antagonizing adenosine receptors in a non-selective manner, caffeine moreover seems to mediate anti-oxidative properties. Dexmedetomidine (1, 5, and 10 μg/kg bodyweight) used for preconditioning showed neuroprotective properties in our model of oxidative stress injury in the developing rat brain, inhibiting apoptotic cell death and pro-inflammatory cytokine insults, improving postnatal neurogenesis and neuronal plasticity. Dexmedetomidine increased the proliferation capacity of mitotic cells, ultimately leading to higher cell numbers of mature neurons without affecting the rate of apoptosis in control animals. The anti-oxidative and anti-inflammatory properties of dexmedetomidine mediated via α2 adrenoreceptor agonism seem to provide a potent potential for neuroprotection. Further investigation into protective drugs with anti-oxidant properties already approved as a drug in neonatal intensive care should continue to be the focus of clinical and experimental studies to better understand pharmacokinetic and molecular mechanisms, and to increase the effectiveness and safety of clinical usage to reconcile unavoidable medically-induced interventions with improved outcomes for premature infants

Super-resolution imaging and estimation of protein copy numbers at single synapses with DNA-PAINT

In the brain, the strength of each individual synapse is defined by the complement of proteins present or the "local proteome." Activity-dependent changes in synaptic strength are the result of changes in this local proteome and posttranslational protein modifications. Although most synaptic proteins have been identified, we still know little about protein copy numbers in individual synapses and variations between synapses. We use DNA-point accumulation for imaging in nanoscale topography as a single-molecule super-resolution imaging technique to visualize and quantify protein copy numbers in single synapses. The imaging technique provides near-molecular spatial resolution, is unaffected by photobleaching, enables imaging of large field of views, and provides quantitative molecular information. We demonstrate these benefits by accessing copy numbers of surface AMPA-type receptors at single synapses of rat hippocampal neurons along dendritic segments

Traceback and Chunk-Based Learning

Recent years have seen increased interest in code-mixing from a usage-based perspective. In usage-based approaches to monolingual language acquisition, a number of methods have been developed that allow for detecting patterns from usage data. In this paper, we evaluate two of those methods with regard to their performance when applied to code-mixing data: the traceback method, as well as the chunk-based learner model. Both methods make it possible to automatically detect patterns in speech data. In doing so, however, they place different theoretical emphases: while traceback focuses on frame-and-slot patterns, chunk-based learner focuses on chunking processes. Both methods are applied to the code-mixing of a German–English bilingual child between the ages of 2;3 and 3;11. Advantages and disadvantages of both methods will be discussed, and the results will be interpreted against the background of usage-based approaches

Neuroinflammation after traumatic injury to the developing brain

PURPOSES: Mechanical trauma to the developing rodent brain induces a diffuse secondary neuroapoptosis associated with infiltration of immune cells, local and systemic increased levels of proinflammatory mediators. Our aim was to study their expression, cellular localization, distribution pattern and time course in various brain regions. MATERIALS AND METHODS: 7-day-old Wistar rats and C57/BL6 mice were subjected to cortical trauma. Animals were sacrificed at defined time points - from 2 h to 14 days following trauma. Brain tissues were processed for molecular analyses, single or double indirect peroxidase/fluorescence immunohistochemistry for apoptotic cell death, microglia and interleukin (IL)-1ß/IL-18. RESULTS: Apoptotic neuronal cell death detected by TUNEL was found at distant regions to trauma site mainly ipsilateral from 6 h to 5 days later. A substantial activation of ED1+ microglia occurred at the site of primary and secondary damages. It was first evident at 12 h, peaked at 36-48 h and decreased significantly after 5 days. A marked increase of mRNA, protein levels and imunohistochemical expression of two pro-inflammatory cytokines, interleukin (IL)-1ß and IL-18, was found from 2 h to 5 days following trauma. Mice deficient in IL-18 (IL-18−/−) were protected against post-traumatic brain damage. CONCLUSIONS: Brain trauma leads to neuroinflammation expressed by microglial activation and an increase in IL-1ß and IL-18. Activated microglia are one of the main cellular sources of elevated levels for both cytokines. They are probably involved in and help sustain apoptotic neurodegeneration over several days after trauma. This finding might define microglia and IL-1ß/IL-18 as potential post-traumatic therapeutic targets

Foreign-language media : Comparison of a German-speaking newspaper for Russian Germans in Russia with a Russian-speaking newspaper in Germany; an analysis

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A Crosslinguistic Study of Child Code-Switching within the Noun Phrase: A Usage-Based Perspective

This paper aims to investigate whether language use can account for the differences in code-switching within the article-noun phrase in children exposed to English and German, French and Russian, and English and Polish. It investigates two aspects of language use: equivalence and segmentation. Four children’s speech is derived from corpora of naturalistic interactions recorded between the ages of two and three and used as a source of the children’s article-noun phrases. We demonstrate that children’s CS cannot be fully explained by structural equivalence in each two languages: there is CS in French-Russian although French does, and Russian does not, use articles. We also demonstrate that language pairs which use higher numbers of articles types, and therefore have more segmented article-noun phrases, are also more open to switching. Lastly, we show that longitudinal use of monolingual articles-noun phrases corresponds with the trends in the use of bilingual article-noun phrases. The German-English child only starts to mix English articles once they become more established in monolingual combinations while the French-Russian child ceases to mix French proto-articles with Russian nouns once target articles enter frequent use. These findings are discussed in the context of other studies which report code-switching across different language pairs