Strasbourg. / Bibliography: p. [89]-91.

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Magister Chirurgiae Dentium (MChD) / Robinson and Martinez first introduced the entity of unicystic ameloblastoma in 1977. Since then numerous case reports and series have been published. The evidence suggests that a more conservative approach can be used successfully to treat the unicystic ameloblastoma. The term unicystic is derived from the macro- and microscopic appearance of the lesion, whereas the term unilocular is used in radiological interpretation to describe a radiolucency having one loculus or compartment. Much confusion stems from the fact that a unicystic ameloblastoma might appear not only as a unilocular lesion, but also as what is often interpreted as a multilocular bone defect.

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Although the visual system is perhaps the most well understood system in the human brain, the precise organization of the neural system whose activity gives rise to higher order functions like visual recognition remains unknown. Furthermore, the manner in which damage involving this system relates to deficit, or the extent to which other factors modulate this relationship is unknown. Building on prior research in this laboratory and elsewhere, which has related focal brain damage to deficits in visual recognition pertaining to particular categories of stimuli, the present study examined both the specificity of lesion-deficit associations, and the relation between damage to the neural systems subserving visual recognition and the severity of a patient's impairment. In the first part, I employed a novel method to address the specificity of visual recognition impairments in relation to the categories of faces, animals, fruits/vegetables and tools/utensils. By using voxelwise logistic regression to parse out variance that could be attributed to deficits across multiple categories, I was able to identify areas that were uniquely predicted by impairment in a single category. In the second part, I examined the relation between the extent of damage in these "category-specific" regions and the severity of the recognition impairment in the same four categories, as well as potential modulating effects from various demographic (e.g., sex, handedness), neuropsychological (e.g., premorbid intellectual functioning, visual-spatial and visuoperceptual ability), and lesion (e.g., age at onset, time elapsed since onset, extent of damage in other ROIs, lesion size) variables. The findings indicated that the largest factor accounting for performance in the recognition of these entities was the extent of damage in the respective category-specific regions. However, within each of the categories, there were additional factors that were also associated with performance, which helped explain some of the additional variance in recognition performance that could not be explained by extent of damage alone. With regard to the latter, I found that damage in certain category-specific regions was related to the severity of deficit across multiple categories, thereby reinforcing the notion of relative specialization within the visual system.

Background: The prevalence of patients with end stage renal disease (ESRD) in Taiwan has risen to the first in the world in recent years. Non-traumatic lower extremity lesion is a common disease of diabetic and ESRD patients. Many studies have found that the prevalence of non-traumatic lower extremity lesion in diabetic patients with ESRD is higher than normal diabetic patients. Prevention the incidence of lower extremity lesions in patients with ESRD may prevent patients from further amputation. Objectives: This study explored the prevalence of ESRD with Non-traumatic lower extremity lesion. We focused on demography status, comorbidities, dialysis therapies and utilization of health care to define the risk factors of disease. Methods: This study conducted secondary data analysis with administrative data from Bureau of National Health Insurance (HV_CD data) for four years (2000, 2002, 2004 and 2006). In total, there were 57021, 75711, 76750, and 86902 for years 2000, 2002, 2004, and 2006, respectively. To attain the research purposes, descriptive analyses and logistic regression were performed. Result: The prevalence of ESRD with non-traumatic lower extremity lesion for the four years were 1.30%, 1.44%, 2.71% and 2.45%, respectively. ESRD patients with and without non-traumatic lower extremity lesion were significant difference between comorbidities (OR for the four years were 2.06, 1.98, 1.86 and 1.83), dialysis therapies (hemodialysis / peritoneal dialysis, OR for the four years were 17.1, 16.79, 15.12 and 9.23) and duration of dialysis (1-5 years / 5 years and more, OR was 1.39 in 2002).There were significant differences in regions of hospital organizations (compared with the north, OR were 0.67 in the center in 2000, 1.47 in the east in 2002 and 0.87 in the center in 2006), class of hospital organizations (compared with Academic Medical Centers, OR were 1.40 in Regional Hospitals, 1.50 in District Hospitals and 0.36 in Physician Clinics in 2000, 0.18 in Physician Clinics in 2002, 0.76 in Regional Hospitals, 0.78 in District Hospitals and 0.23 in Physician Clinics in 2004, 0.66 in Regional Hospitals, 0.75 in District Hospitals and 0.26 in Physician Clinics in 2006 ) and outpatient visits ( positive correlation in all years except 2000). Conclusion: The risk factors of suffering non-traumatic lower extremity lesion in ESRD patients are comorbidities, dialysis therapies and duration of dialysis. In the part of regions of hospital organizations, the east region has higher and the center region has lower probability of suffering the disease, comparing with the north region. Academic Medical Centers has the highest probability to find ESRD patients with non-traumatic lower extremity lesion. We also found the numbers of outpatient visits were increasing with the disease. Based on the results, we highly suggest that caregivers from dialysis units have to pay great attention in taking care of the ESRD patients with non-traumatic lower extremity lesion to prevent from the further amputation.

The current prevailing notion is that the limbic system is inextricably linked to emotion, and indeed, most textbooks, research articles, and scientific lectures tout the limbic system as being the predominant purveyor of emotional processing in the brain. Yet, more than a half-century of research has produced surprisingly little evidence in support of such a notion, suggesting that the concept of an emotional limbic system is overly simplistic. The primary objective of this thesis is to determine whether the limbic system is necessary for one aspect of emotion, namely, its conscious experience. Neurological patients with focal damage to different regions of the limbic system - including the hippocampus, amygdala, insular cortex, anterior cingulate cortex (ACC), and ventromedial prefrontal cortex (vmPFC) - underwent multiple emotion induction procedures using affectively-laden film clips. For comparison, two other groups of participants were tested: patients with brain damage outside of the limbic system and healthy participants without brain damage. Two emotion inductions aimed at eliciting diffuse emotional states of positive or negative affect, and five emotion inductions aimed at eliciting specific emotional states of happiness, sadness, anger, disgust, or fear. Immediately following the end of each film clip, the return of emotion back to its baseline state was tracked over a three minute "emotion recovery" time period. The results of the experiment revealed three main findings. First, limbic system damage did not disrupt the experience of emotion during the film clips, with patients reporting high levels of the induced target emotion at a magnitude comparable to both comparison groups. Second, patients with bilateral damage circumscribed to either the hippocampus or the vmPFC demonstrated an abnormally slow rate of emotion recovery, indicating that these limbic regions are important for the successful downregulation of emotion. Third, patients with large bilateral lesions affecting multiple limbic structures (including the medial temporal lobes and insular cortices) showed an abnormally rapid rate of emotion recovery, with the induced emotion returning to baseline levels within 60 seconds following the end of each film. Based on these findings, it is concluded that the limbic system is not necessary for the experience of emotion, but is necessary for sustaining and regulating that experience after the emotion-inducing stimulus is no longer directly accessible to consciousness.

To examine the effect of a central noradrenergic lesion on the reactivity of the 5-HT1B receptor we compared intact male rats with rats in which noradrenergic nerve terminals were largely destroyed with the neurotoxin DSP-4 (50 mg/kg × 2, on the 1st and 3rd days of postnatal life). When rats attained 10 weeks of age, control and DSP-4 rats were divided into two subgroups receiving either saline or the serotonin (5-HT) synthesis inhibitor (p-chlorophenylalanine; p-CPA; 100 mg/kg). Employing an elevated plus maze test, we demonstrated that CP 94,253 (5-propoxy-3-(1,2,3,6-tetrahydro-4-pyridinyl)-1H-pyrrolo[3,2-b]pyridine hydrochloride)(4.0 mg/kg; 5-HT1B agonist) induced an anxiogenic-like action in control rats; however, it failed to elicit this effect in the DSP-4 group. Surprisingly, in p-CPApretreated rats anxiogenic-like activity was observed both in control and DSP-4 treated rats. CP 94,253 significantly attenuated 5-HT synthesis in the medial prefrontal cortex (mPFC) of control rats, and SB 216641 (N-{3-[3-(dimethylamino) ethoxy]-4-methoxyphenyl}-2'-methyl-4'-(5-methyl-1,2,4-oxadiazol-3-yl)-[1,1'-biphenyl]-4-carboxamide hydrochloride) (4.0 mg/kg; 5-HT1B antagonist) was able to antagonize this effect. Conversely, CP 94,253 failed to significantly inhibit the 5-HT synthesis rate in DSP-4-treated rats. In the microdialysis study CP 94,253 induced long-lasting attenuation of 5-HT release in the mPFC of control rats but had no effect in DSP-4 rats. These data lead to the proposal that presynaptic 5-HT1B autoreceptors underwent desensitization in DSP-4 treated rats.

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