Kielitaju kielitieteessä:introspektion ja intuition tarkastelua

Tiivistelmä. Tarkastelen tieteenfilosofisessa pro gradu -tutkielmassani introspektiota ja intuitiota, jotka ovat kielitieteen keskeisiä käsitteitä. Keskeisyydestään huolimatta tai juuri siitä johtuen introspektio ja intuitio esiintyvät tutkimuskirjallisuudessa tavanomaisesti itsestäänselvinä käsitteinä. Käsiteparin sisältöä selventääkseni määrittelen tutkielmassani kielitajun käsitteen, joka yhdistää introspektiota ja intuitiota. Kielitaju on ihmisen luontainen ja määrittävä ominaisuus, jonka kautta hän kokee maailmaa. Se käsittää ihmisen kyvyn tuottaa, tulkita, käyttää, jakaa ja luoda kieltä. Kielitaju on kielellisyyttä, merkitysten antamista ja niiden näkemistä ympäröivässä maailmassa. Siten se on erottamaton osa kielentutkimusta, mihin viitataan useissa kielitieteellisissä julkaisuissa. Introspektio ja intuitio ovat kielitajun spesifejä käyttötapoja kielitieteessä. Kielitajun kautta määriteltyinä introspektio on kysymysten esittämistä omalle kielitajulle ja intuitio on kielitajulta saatu vastaus. Täydennän introspektion ja intuition määritelmiä niiden prototyyppisillä piirteillä, jotka rajasin kielitieteellisestä tutkimuskirjallisuudesta käyttäen nelivaiheista käsiteanalyysia. Introspektion ja intuition prototyyppiset piirteet kertovat, kuka kielitajua prototyyppisesti käyttää osana kielitieteellistä tutkimusta, mitä käyttötarkoitusta varten ja millä tavoin. Introspektion ja intuition prototyyppiset piirteet ovat antonyymisia eli toistensa vastakohtia. Introspektion prototyyppiset piirteet ovat YKSILÖ, VÄLINE ja VÄLILLINEN, ja intuition prototyyppiset piirteet ovat niiden vastaparit KOLLEKTIIVI, AINEISTO ja VÄLITÖN. Introspektion prototyyppiset piirteet tiivistyvät tutkijaan ja tämän rooliin kielitieteen harjoittajana, ja intuition piirteet kiteytyvät kieliyhteisöön kollektiivisena aineiston tarjoajana. Prototyyppisillä piirteillä täydennetyt introspektion ja intuition määritelmät ovat seuraavat: Introspektio on kysymysten esittämistä omalle kielitajulle. Prototyyppisesti kysymyksiä esittää kielitieteellisessä tutkimuksessa tutkija, joka tutkii kieltä tietoisesti kielitaju välineenään. Intuitio on vastaus kielitajulle esitettyyn kysymykseen. Prototyyppisesti vastauksia hankitaan kielitieteellisessä tutkimuksessa kieliyhteisöltä osana tutkimusasetelmaa. Kollektiivinen kieliyhteisö tarjoaa tutkimukselle prosessoimattoman ja monipuolisen aineiston. Näkökulmasta riippuen introspektion ja intuition piirteitä voidaan pitää kielitieteen kannalta joko edullisina tai epäedullisina. Tutkielman toisessa osassa syvennyn kielitieteen arvoihin ja ihanteisiin, jotka vaikuttavat introspektion ja intuition vastaanottoon. Tieteellä on yleisiä arvoja, joita tutkimuksessa pyritään noudattamaan mahdollisimman hyvin. Määrittelen nämä arvot hyviksi selityksiksi sekä rehellisyydeksi, objektiivisuudeksi, kriittisyydeksi, avoimuudeksi ja julkisuudeksi. Yleisten arvojen tulkinta riippuu kontekstuaalisista arvoista. Ne ovat henkilökohtaisia, sosiaalisia ja kulttuurisia preferenssejä sille, kuinka tieteen yleiset arvot voidaan parhaiten täyttää. Eri aikoina ja eri tiedeyhteisöissä on omat näkemyksensä siitä, kuinka hyvää kielitiedettä harjoitetaan. Ihanteiden muuttuessa vuoroin introspektiota ja vuoroin intuitiota on pidetty arvossa. Tämän hetken kielitieteen ihanteiksi on määritelty aineiston monipuolisuus sekä aineiston oikeanlainen käsittely. Nykypäivän ihanteita edustamaan valitsin lähempään tarkasteluun András Kertészin ja Csilla Rákosin kehittämän p-mallin. P-mallissa muotoillaan uudenlaiset lähtökohdat kielitieteelliselle tutkimukselle, jotta kieli kompleksina tutkimuskohteena tulee edustetuksi mahdollisimman hyvin. P-mallin lähtökohdat ovat epävarmuus, uskottavuus, syklisyys, prismaattisuus, epäjohdonmukaisuus ja pluraalisuus sekä uskottava argumentointi. Tästä näkökulmasta katsottuna yksikään aineiston laji tai metodi ei ole ylitse muiden. Jokaisella niistä on paikkansa kielitieteessä, sillä ne täydentävät toinen toistaan. Introspektio ja intuitio ovat saman kolikon kaksi puolta, ja käsitteen vahvuus on yhtä lailla sen heikkous. Introspektio ja tutkija loistaa yksilöllisenä ja välillisenä välineenä tutkimuksessa, siinä missä intuitio ja kieliyhteisö ovat oiva ja välitön kollektiivisen aineiston lähde. Introspektion ja intuition tarkastelu prototyyppisten piirteiden sekä arvojen ja ihanteiden näkökulmasta tarjoaa uudenlaisen näkymän kielitieteeseen ja sen tieteenfilosofiaan sekä metodologiaan. Introspektio ja intuitio edustavat kielitiedettä pienoiskoossa, ja niitä tutkimalla tulee tarkastelleeksi koko tieteenalaa. Introspektion ja intuition käsittelystä päätellen kielitieteelle vaikuttaa hahmottuvan uusi ihanne, jota kutsun solidaarisuudeksi. Kielitieteen kehittymisen ja menestyksen nähdään olevan sidoksissa yhteistyöhön, ymmärrykseen ja kunnioittamiseen, jotka eivät koske ainoastaan metodiikkaa vaan myös kielentutkimuksen eri lajeja ja tutkijoita niiden takana

A truncated laminin chain homologous to the B2 chain: structure, spatial expression, and chromosomal assignment

We describe the identification of a novel laminin chain. Overlapping clones were isolated from a human fibrosarcoma HT1080 cell cDNA library spanning a total of 5,200 bp. A second set of clones contained an alternative 3' end sequence giving a total of 4,316 bp. The longer sequence contained an open reading frame for a 1,193-residue-long polypeptide. The alternative sequence was shortened at the carboxyl-terminal end coding for a 1,111-residue-long polypeptide. The amino acid sequence contained 21 amino acids of a putative signal peptide and 1,172 residues or alternatively 1,090 residues of a sequence with five distinct domains homologous to domains I-V in laminin chains. Comparison of the amino acid sequences showed that the novel laminin chain is homologous to the laminin B2 chain. However, the structure of the novel laminin chain isolated here differs significantly from that of the B2 chain in that it has no domain VI and domains V, IV, and III are shorter, resulting in a truncated laminin chain. The alternative sequence had a shortened domain I/II. In accordance with the current nomenclature, the chain characterized here is termed B2t. Calculation of possible chain interactions of laminin chains with the B2t chain domain I/II indicated that the B2t chain can replace the B2 chain in some laminin molecules. The gene for the laminin B2t chain (LAMB2T) was localized to chromosome 1q25-q31 in close proximity to the laminin B2 chain gene. Northern analysis showed that the B2t chain is expressed in several human fetal tissues but differently from the laminin B1 and B2 chains. By in situ hybridization expression of the B2t chain was localized to specific epithelial cells in skin, lung, and kidney as opposed to a general epithelial and endothelial cell expression of the laminin B2 chain in the same tissues

Competing mechanisms for step meandering in unstable growth

The meander instability of a vicinal surface growing under step flow conditions is studied within a solid-on-solid model. In the absence of edge diffusion the selected meander wavelength agrees quantitatively with the continuum linear stability analysis of Bales and Zangwill [Phys. Rev. B {\bf 41}, 4400 (1990)]. In the presence of edge diffusion a local instability mechanism related to kink rounding barriers dominates, and the meander wavelength is set by one-dimensional nucleation. The long-time behavior of the meander amplitude differs in the two cases, and disagrees with the predictions of a nonlinear step evolution equation [O. Pierre-Louis et al., Phys. Rev. Lett. {\bf 80}, 4221 (1998)]. The variation of the meander wavelength with the deposition flux and with the activation barriers for step adatom detachment and step crossing (the Ehrlich-Schwoebel barrier) is studied in detail. The interpretation of recent experiments on surfaces vicinal to Cu(100) [T. Maroutian et al., Phys. Rev. B {\bf 64}, 165401 (2001)] in the light of our results yields an estimate for the kink barrier at the close packed steps.Comment: 8 pages, 7 .eps figures. Final version. Some errors in chapter V correcte

Asymptotic step profiles from a nonlinear growth equation for vicinal surfaces

We study a recently proposed nonlinear evolution equation describing the collective step meander on a vicinal surface subject to the Bales-Zangwill growth instability [O. Pierre-Louis et al., Phys. Rev. Lett. (80), 4221 (1998)]. A careful numerical analysis shows that the dynamically selected step profile consists of sloped segments, given by an inverse error function and steepening as sqrt(t), which are matched to pieces of a stationary (time-independent) solution describing the maxima and minima. The effect of smoothening by step edge diffusion is included heuristically, and a one-parameter family of evolution equations is introduced which contains relaxation by step edge diffusion and by attachment-detachment as special cases. The question of the persistence of an initially imposed meander wavelength is investigated in relation to recent experiments.Comment: 4 pages, 5 included figures. Typo in Eq.(5) corrected, section headlines added and Ref.[12] update

Morphology of ledge patterns during step flow growth of metal surfaces vicinal to fcc(001)

The morphological development of step edge patterns in the presence of meandering instability during step flow growth is studied by simulations and numerical integration of a continuum model. It is demonstrated that the kink Ehrlich-Schwoebel barrier responsible for the instability leads to an invariant shape of the step profiles. The step morphologies change with increasing coverage from a somewhat triangular shape to a more flat, invariant steady state form. The average pattern shape extracted from the simulations is shown to be in good agreement with that obtained from numerical integration of the continuum theory.Comment: 4 pages, 4 figures, RevTeX 3, submitted to Phys. Rev.

A mouse model of the schizophrenia-associated 1q21.1 microdeletion syndrome exhibits altered mesolimbic dopamine transmission

Abstract 1q21.1 hemizygous microdeletion is a copy number variant leading to eightfold increased risk of schizophrenia. In order to investigate biological alterations induced by this microdeletion, we generated a novel mouse model (Df(h1q21)/+) and characterized it in a broad test battery focusing on schizophrenia-related assays. Df(h1q21)/+ mice displayed increased hyperactivity in response to amphetamine challenge and increased sensitivity to the disruptive effects of amphetamine and phencyclidine hydrochloride (PCP) on prepulse inhibition. Probing of the direct dopamine (DA) pathway using the DA D1 receptor agonist SKF-81297 revealed no differences in induced locomotor activity compared to wild-type mice, but Df(h1q21)/+ mice showed increased sensitivity to the DA D2 receptor agonist quinpirole and the D1/D2 agonist apomorphine. Electrophysiological characterization of DA neuron firing in the ventral tegmental area revealed more spontaneously active DA neurons and increased firing variability in Df(h1q21)/+ mice, and decreased feedback reduction of DA neuron firing in response to amphetamine. In a range of other assays, Df(h1q21)/+ mice showed no difference from wild-type mice: gross brain morphology and basic functions such as reflexes, ASR, thermal pain sensitivity, and motor performance were unaltered. Similarly, anxiety related measures, baseline prepulse inhibition, and seizure threshold were unaltered. In addition to the central nervous system-related phenotypes, Df(h1q21)/+ mice exhibited reduced head-to tail length, which is reminiscent of the short stature reported in humans with 1q21.1 deletion. With aspects of both construct and face validity, the Df(h1q21)/+ model may be used to gain insight into schizophrenia-relevant alterations in dopaminergic transmission

Activation of c-Jun N-Terminal Kinase (JNK) during Mitosis in Retinal Progenitor Cells

Most studies of c-Jun N-terminal Kinase (JNK) activation in retinal tissue were done in the context of neurodegeneration. In this study, we investigated the behavior of JNK during mitosis of progenitor cells in the retina of newborn rats. Retinal explants from newborn rats were kept in vitro for 3 hours and under distinct treatments. Sections of retinal explants or freshly fixed retinal tissue were used to detect JNK phosphorylation by immunohistochemistry, and were examined through both fluorescence and confocal microscopy. Mitotic cells were identified by chromatin morphology, histone-H3 phosphorylation, and location in the retinal tissue. The subcellular localization of proteins was analyzed by double staining with both a DNA marker and an antibody to each protein. Phosphorylation of JNK was also examined by western blot. The results showed that in the retina of newborn rats (P1), JNK is phosphorylated during mitosis of progenitor cells, mainly during the early stages of mitosis. JNK1 and/or JNK2 were preferentially phosphorylated in mitotic cells. Inhibition of JNK induced cell cycle arrest, specifically in mitosis. Treatment with the JNK inhibitor decreased the number of cells in anaphase, but did not alter the number of cells in either prophase/prometaphase or metaphase. Moreover, cells with aberrant chromatin morphology were found after treatment with the JNK inhibitor. The data show, for the first time, that JNK is activated in mitotic progenitor cells of developing retinal tissue, suggesting a new role of JNK in the control of progenitor cell proliferation in the retina

Oxidant-NO dependent gene regulation in dogs with type I diabetes: impact on cardiac function and metabolism

<p>Abstract</p> <p>Background</p> <p>The mechanisms responsible for the cardiovascular mortality in type I diabetes (DM) have not been defined completely. We have shown in conscious dogs with DM that: <it>1</it>) baseline coronary blood flow (CBF) was significantly decreased, <it>2</it>) endothelium-dependent (ACh) coronary vasodilation was impaired, and <it>3</it>) reflex cholinergic NO-dependent coronary vasodilation was selectively depressed. The most likely mechanism responsible for the depressed reflex cholinergic NO-dependent coronary vasodilation was the decreased bioactivity of NO from the vascular endothelium. The goal of this study was to investigate changes in cardiac gene expression in a canine model of alloxan-induced type 1 diabetes.</p> <p>Methods</p> <p>Mongrel dogs were chronically instrumented and the dogs were divided into two groups: one normal and the other diabetic. In the diabetic group, the dogs were injected with alloxan monohydrate (40-60 mg/kg iv) over 1 min. The global changes in cardiac gene expression in dogs with alloxan-induced diabetes were studied using Affymetrix Canine Array. Cardiac RNA was extracted from the control and DM (n = 4).</p> <p>Results</p> <p>The array data revealed that 797 genes were differentially expressed (P < 0.01; fold change of at least ±2). 150 genes were expressed at significantly greater levels in diabetic dogs and 647 were significantly reduced. There was no change in eNOS mRNA. There was up regulation of some components of the NADPH oxidase subunits (gp91 by 2.2 fold, P < 0.03), and down-regulation of SOD1 (3 fold, P < 0.001) and decrease (4 - 40 fold) in a large number of genes encoding mitochondrial enzymes. In addition, there was down-regulation of Ca²⁺cycling genes (ryanodine receptor; SERCA2 Calcium ATPase), structural proteins (actin alpha). Of particular interests are genes involved in glutathione metabolism (glutathione peroxidase 1, glutathione reductase and glutathione S-transferase), which were markedly down regulated.</p> <p>Conclusion</p> <p>our findings suggest that type I diabetes might have a direct effect on the heart by impairing NO bioavailability through oxidative stress and perhaps lipid peroxidases.</p

Stat3 controls cell death during mammary gland involution by regulating uptake of milk fat globules and lysosomal membrane permeabilization.

We have previously demonstrated that Stat3 regulates lysosomal-mediated programmed cell death (LM-PCD) during mouse mammary gland involution in vivo. However, the mechanism that controls the release of lysosomal cathepsins to initiate cell death in this context has not been elucidated. We show here that Stat3 regulates the formation of large lysosomal vacuoles that contain triglyceride. Furthermore, we demonstrate that milk fat globules (MFGs) are toxic to epithelial cells and that, when applied to purified lysosomes, the MFG hydrolysate oleic acid potently induces lysosomal leakiness. Additionally, uptake of secreted MFGs coated in butyrophilin 1A1 is diminished in Stat3-ablated mammary glands and loss of the phagocytosis bridging molecule MFG-E8 results in reduced leakage of cathepsins in vivo. We propose that Stat3 regulates LM-PCD in mouse mammary gland by switching cellular function from secretion to uptake of MFGs. Thereafter, perturbation of lysosomal vesicle membranes by high levels of free fatty acids results in controlled leakage of cathepsins culminating in cell death.This work was supported by a grant from the Medical Research Council programme grant no. MR/J001023/1 (T.J.S. and B. L-L.) and a Cancer Research UK Cambridge Cancer Centre PhD studentship (H.K.R.).This is the accepted manuscript. The final version is available from Nature Publishing at http://www.nature.com/ncb/journal/vaop/ncurrent/full/ncb3043.html

JunD/AP-1-Mediated Gene Expression Promotes Lymphocyte Growth Dependent on Interleukin-7 Signal Transduction

Interleukin-7 (IL-7) is an essential cytokine for lymphocyte growth that has the potential for promoting immune reconstitution. This feature makes IL-7 an ideal candidate for therapeutic development. As with other cytokines, signaling through the IL-7 receptor induces the JAK/STAT pathway. However, the broad scope of IL-7 regulatory targets likely necessitates the use of other signaling components whose identities remain poorly defined. To this end, we used an IL-7 dependent T-cell line to examine how expression of the glycolytic enzyme, Hexokinase II (HXKII) was regulated by IL-7 in a STAT5-independent manner. Our studies revealed that IL-7 promoted the activity of JNK (Jun N-terminal Kinase), and that JNK, in turn, drove the expression of JunD, a component of the Activating Protein 1 (AP-1) transcription factors. Gel shifts showed that the AP-1 complex induced by IL-7 contained JunD but not c-Fos or c-Jun. Inhibition of JNK/JunD blocked glucose uptake and HXKII gene expression, indicating that this pathway was responsible for promoting HXKII expression. Because others had shown that JunD was a negative regulator of cell growth, we performed a bioinformatics analysis to uncover possible JunD-regulated gene targets. Our search revealed that JunD could control the expression of proteins involved in signal transduction, cell survival and metabolism. One of these growth promoters was the oncogene, Pim-1. Pim-1 is an IL-7-induced protein that was inhibited when the activities of JNK or JunD were blocked, showing that in IL-7 dependent T-cells JunD can promote positive signals transduced through Pim-1. This was confirmed when the IL-7-induced proliferation of CD8 T-cells was impaired upon JunD inhibition. These results show that engagement of the IL-7 receptor drives a signal that is more complex than the JAK/STAT pathway, activating JNK and JunD to induce rapid growth stimulation through the expression of metabolic and signaling factors like HXKII and Pim-1