Creating A New Automotive Exterior Design Approach Model: The Relationship Between Form And Body Color Qualities

This study creates a New Automotive Exterior Design Approach Model. Form and body color qualities are objectified (quantified) in order to grasp unspoken subjective customer impressions (preferences). Related cause-and-effect relationships are then clarified. This is done with the help of statistics, which are used to identify the main elements that younger buyers are looking for in automotive body colors. Next, a survey is conducted using painted panels to find out what color elements generate subjective customer impressions. Line-of-sight analysis and 3D-CAD software are used to assign numerical values to form and color, while research-oriented CAD models and biometric devices are used to quantify the impact that form and color have on subjective customer impressions. The insights gained from this are then used to understand the relationship between survey data assessing subjective impressions and qualities of form and body color. The resulting knowledge is then applied to optimally match form and body color in a way that customers find attractive. The desired results are obtained

The A-VEDAM Model For Approaching Vehicle Exterior Design

The exterior design of a vehicle is an important subjective factor in customer purchase decisions today, and it is critical that designs match customer lifestyles. This paper introduces A-VEDAM (Amasakalab’s Vehicle Exterior design Approach Model), a model for approaching exterior design in a way that harmonizes the external form (profile) and color of the vehicle to meet the demands of the coming years. The development of the A-VEDAM focuses on the fact that more young women are getting driver’s licenses and purchasing cars

Recovery of atrophic parotid glands in rats fed a liquid diet by switching to a pellet diet

Objective: In this study, we aimed to clarify how parotid glands, made atrophic by a liquid diet, recover after diet change. Design: Seven-week-old male Wistar rats were fed a pellet (control group) or a liquid diet (experimental group) for the first 14 days. Thereafter, all animals were fed a pellet diet for up to 14 days (days 0-14). The parotid glands were removed, weighed and examined histologically and ultrastructurally. Immunohistochemistry was performed for BrdU, a marker of proliferating cells, and Casp-3, a marker of apoptotic cells. Results: Feeding of a liquid diet for 14 days induced atrophy of the parotid glands. Histologically, acinar cells were small on day 0, compared with the control group. After changing the diet from liquid to pellet form, acinar cells increased in size over time, recovering nearly fully by day 7. Many BrdU-positive acinar cells were observed in the glands in the experimental group on days 1 and 3. Although more acinar cells were Casp-3-positive compared with the control group on day 0, there was no difference between the two groups after the diet change. Ultrastructurally, the cellular organelles did not exhibit a substantial alteration, except for an increase in secretory granules following diet change. Conclusions: Our findings suggest that atrophic parotid glands are able to recover to their normal size by switching the diet from liquid to pellet form and that an increase in both the size and number of acinar cells plays an important role in this recovery process

OFDM伝送における送信電力制御を用いた非線形ひずみ抑圧法に関する研究

早大学位記番号:新6867早稲田大

Dna Damage And Repair In Rat Epidermal Keratinocytes (polyamines, Differentiation).

Newborn rat cutaneous epidermal keratinocytes were grown under conditions that did or did not favor differentiation. Cultures were exposed to N-methyl-N'-nitro-N-nitroso-guanidine (MNNG) or to bis-chloro-ethylsulfide (BCES). DNA damage (alkali-labile lesions, single-strand breaks, and cross-links) was measured with an assay which uses alkaline unwinding of DNA and hydroxylapatite chromatography. DNA repair was inferred from the disappearance of DNA damage over time. MNNG caused dose-dependent DNA single-strand breaks at concentrations from 10 to 30 (mu)M in non-differentiated cells (L-culture) and differentiated cells (N-culture). The rate of DNA repair was inversely related to the concentration of MNNG. L- and N-cultures differed significantly in susceptibility to MNNG-induced DNA damage and its repair. BCES caused dose-dependent cross-links at concentrations from 1 to 200 (mu)M in both L- and N-cultures. DNA damage induced by 5 (mu)M BCES was repaired within 48 hr in N-culture (differentiated cells), while L-culture (non-differentiated cells) could not repair the 5 (mu)M BCES-induced DNA damage. DNA repair was inhibited in both L- and N-cultures by aphidicolin (Apc), a potent inhibitor of DNA polymerase alpha. The results of studies of DNA repair inhibition by Apc suggest that DNA polymerase alpha is involved in repair synthesis for BCES-induced damage. Cellular polyamine levels were increased by supplementation with exogenous polyamines or depleted by treatment with alpha-difluoromethylornithine (DFMO). With control DS-DNA normalized to 100%, 5 (mu)M BCES-induced crosslinking was inhibited in polyamine pretreated N-culture, resulting 91.6 (+OR-) 1.58% DS-DNA, while L-culture had 118.6 (+OR-) 1.76% DS-DNA, suggesting BCES-induced crosslinking. This differential susceptibility of L- and N-cultures to BCES-induced DNA crosslinking was highly correlated with cellular polyamine levels. N-culture had a 2-fold increase in spermidine levels and an 8-fold increase in spermine levels compared to L-culture after 5 days exogenous putrescine supplementation. DFMO pretreated L- and N-cultures suffered BCES-induced crosslinking due to depleted polyamine levels. Therefore, the protective effects of polyamines on BCES-induced crosslinking were specific for N-culture (differentiated cells). Polyamine supplementation did not markedly alter MNNG-induced DNA damage not its repair in either L- or N-culture.Ph.D.Biological SciencesMolecular biologyUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/127979/2/8702797.pd

Histological aspect of the effects of soft food on major salivary glands

The modern Japanese population favors soft foods, which do not demand extensive mastication. However, daily intake of soft foods is considered to have unfavorable influences on the mind and body. This is especially within the oral maxillofacial region. Consequently, many studies using experimental animals, feed a liquid or powdered diet and indicate that soft foods negatively affect the jaw bones, masseter muscle, and temporomandibular joint. Furthermore, since a report by Hall and Schneyer in 1964, the effects of soft foods on salivary glands have been under investigation. Soft food intake induces atrophic alteration to the parotid glands in adult animals. In these glands, shrinkage, suppression of proliferation, and apoptotic deletion of acinar cells were observed. In growing animals fed soft foods, parotid gland growth is inhibited through the suppression of an increase of acinar cell size and of acinar cell proliferation, but not through apoptosis. These findings support that unfavorable effects on parotid glands are induced by the intake of soft food regardless of growing or mature phases. However, different observations exist between these two phases. Despite accumulated knowledge on parotid glands, the debate whether soft food affects submandibular and sublingual glands remains controversial. It is the case that many studies agree soft food unfavorably affects parotid glands to a greater extent than submandibular and sublingual glands. This article reviews the histological effects of soft food on major salivary glands and introduces recent data from our research group