Scales, Implicatures, and in fact, if not, and let alone Constructions.

太田朗先生傘寿記念論文

Multimodal design : the semiotic resources of children's graphic representation

In asking how children's graphic representation can be understood as multimodal design, I argue that meaning-making is a complex process of semiotic interweaving. My definition of graphic representation for this thesis embraces the full range of marks made on any graphic surface. Multimodal design is the socioculturally shaped process of transformation where existing semiotic (meaning-making) resources are chosen, shaped and combined according to the individual's interest and his or her perception of the particular representational or communicational need. I propose that graphic representation might be thought about as multimodal compounds (co-present writing and image) and multimodal composites (an integration of the modes that make up the self-contained entities of writing and image). I explore how texts can be understood multimodally by examining what the semiotic resources of children's graphic representation are, how they carry meaning and how they interrelate. Through in-depth analysis of writing and drawing both discretely and appearing together in the same graphic text, I analyse paper-based and electronic texts produced at home and school for different purposes. I take my interpretations of the signs children have made and my theorization always to be hypotheses. Language-as-writing and drawing-as-image offer potentialities for different ways of making meaning but common and particularized semiotic modes such as presentation, layout and punctuation operate across graphic representation. These modes work together in a semiotic partnership. I suggest that semiotic principles across modes of communication including and going beyond the graphic might include criteriality, connectivity and salience. This implies the notion of a multimodal disposition. The multimodality of children's graphic representational design has implications for pedagogy, curriculum policy, professional development and the research community.

Modifiable Etiological Factors and the Burden of Stroke from the Rotterdam Study: A Population-Based Cohort Study

<div><p>Background</p><p>Stroke prevention requires effective treatment of its causes. Many etiological factors for stroke have been identified, but the potential gain of effective intervention on these factors in terms of numbers of actually prevented strokes remains unclear because of the lack of data from cohort studies. We assessed the impact of currently known potentially modifiable etiological factors on the occurrence of stroke.</p><p>Methods and Findings</p><p>This population-based cohort study was based on 6,844 participants of the Rotterdam Study who were aged ≥55 y and free from stroke at baseline (1990–1993). We computed population attributable risks (PARs) for individual risk factors and for risk factors in combination to estimate the proportion of strokes that could theoretically be prevented by the elimination of etiological factors from the population.</p><p>The mean age at baseline was 69.4 y (standard deviation 6.3 y). During follow-up (mean follow-up 12.9 y, standard deviation 6.3 y), 1,020 strokes occurred. The age- and sex-adjusted combined PAR of prehypertension/hypertension, smoking, diabetes mellitus, atrial fibrillation, coronary disease, and overweight/obesity was 0.51 (95% CI 0.41–0.62) for any stroke; hypertension and smoking were the most important etiological factors. C-reactive protein, fruit and vegetable consumption, and carotid intima-media thickness in combination raised the total PAR by 0.06. The PAR was 0.55 (95% CI 0.41–0.68) for ischemic stroke and 0.70 (95% CI 0.45–0.87) for hemorrhagic stroke.</p><p>The main limitations of our study are that our study population comprises almost exclusively Caucasians who live in a middle and high income area, and that risk factor awareness is higher in a study cohort than in the general population.</p><p>Conclusions</p><p>About half of all strokes are attributable to established causal and modifiable factors. This finding encourages not only intervention on established etiological factors, but also further study of less well established factors.</p><p><i>Please see later in the article for the Editors' Summary</i></p></div

Population attributable risks of presumed etiological factors for any stroke: women (<i>n/N</i> = 614/4,112).

a<p>All analyses are adjusted for age, sex, hypertension, smoking, atrial fibrillation, and diabetes mellitus, if appropriate.</p><p>n.a., not applicable because the hazard ratio is smaller than one.</p

Relationship between the etiological factors described in the 2011 American Heart Association/American Stroke Association guidelines [3] and the etiological factors used in our study.

<p>The classification into well-documented and modifiable risk factors versus less well-documented or potentially modifiable risk factors is adopted from the guidelines.</p

Population attributable risks of presumed etiological factors for which data were available only for subgroups, for any stroke: men and women.

a<p>All analyses are adjusted for age, sex, hypertension, smoking, diabetes mellitus, atrial fibrillation, coronary disease, and overweight/obesity, if appropriate.</p>b<p>Total PAR based on hypertension, smoking, diabetes mellitus, atrial fibrillation, coronary disease, and overweight/obesity, calculated in this subgroup of the study population.</p>c<p>Very low intake (<3 servings per day) and low intake (3–5 servings per day) versus adequate intake (>5 servings per day) of fruits and/or vegetables.</p

Studies reporting total population attributable risk for stroke.

<p>Studies reporting total population attributable risk for stroke.</p

Population attributable risks of presumed etiological factors for any stroke: women (<i>n/N</i> = 614/4,112).

a<p>All analyses are adjusted for age, sex, hypertension, smoking, atrial fibrillation, and diabetes mellitus, if appropriate.</p><p>n.a., not applicable because the hazard ratio is smaller than one.</p

Population attributable risks of presumed etiological factors for any stroke: men (<i>n/N</i> = 406/2,732).

a<p>All analyses are adjusted for age, sex, hypertension, smoking, atrial fibrillation, and diabetes mellitus, if appropriate.</p

Population attributable risks of presumed etiological factors for which data were available only for subgroups, for any stroke (<i>n/N</i> = 545/3,570).

<p>Category boundaries for C-reactive protein quartiles were 0.896, 1.900, and 3.960 for men and 0.902, 1.830, and 3.360 for women. Category boundaries for carotid IMT quartiles were 0.72, 0.80, and 0.92 for men and 0.67, 0.76, and 0.85 for women.</p>a<p>All analyses are adjusted for age, sex, hypertension, smoking, diabetes mellitus, atrial fibrillation, coronary disease, and overweight/obesity, if appropriate.</p>b<p>Total PAR based on hypertension, smoking, diabetes mellitus, atrial fibrillation, coronary disease, and overweight/obesity, calculated in this subgroup of the study population.</p><p>n.a., not applicable because the hazard ratio is smaller than one.</p