Improving electronics with use: design to wear

Today\u27s products are designed to exude high fashion and flawless beauty, which are inevitably susceptible to deterioration over time, making the aesthetic value disappear due to wear and tear. The purpose of this thesis is to design modern products not only to improve their aesthetic value and meaning but also their usability, while taking advantage of wear and tear in order to improve value. The majority of previous studies focused on preventing the deterioration of products, whereas, this thesis approaches the opposite view of allowing wear to boost the product\u27s value, thereby improving functionality with desirable appearance by design. The electronics industry, with its constant technological advances, encourages an increasingly rapid obsolescence of goods and, therefore, consumers yearn for new goods with updated technology and a more attractive appearance. In this paper, I will discuss the marketing strategy known as planned obsolescence. I will look at the meaning of goods in a material culture to analyze the current situation and provide insight into the value of goods and human interaction during the use process. I will focus on wear and design factors to address new possibilities for a desirable experience and beauty from deterioration of the product. I will then conclude by proposing a prototype of a digital camera that accrues increasingly desirable beauty and functionality throughout its use. Quantitative research and qualitative research were used to identify problems and defined the way the problems are solved

Invisible dark gauge boson search in top decays using a kinematic method

We discuss the discovery potential of a dark force carrier ($Z'$) of very light mass, $m_{Z'} \lesssim {\cal O}(1-10)$ GeV, at hadron colliders via rare top quark decays, especially when it decays invisibly in typical search schemes. We emphasize that the top sector is promising for the discovery of new particles because top quark pairs are copiously produced at the Large Hadron Collider. The signal process is initiated by a rare top decay into a bottom quark and a charged Higgs boson ($H^\pm$) decaying subsequently into a $W$ and one or multiple $Z'$s. The light $Z'$ can be invisible in collider searches in various scenarios, and it would be hard to distinguish the relevant collider signature from the regular $t\bar{t}$ process in the Standard Model. We suggest a search strategy using the recently proposed on-shell constrained $M_2$ variables. Our signal process is featured by an $\textit{asymmetric}$ event topology, while the $t\bar{t}$ is $\textit{symmetric}$. The essence behind the strategy is to evoke some contradiction in the relevant observables by applying the kinematic variables designed under the assumption of the $t\bar{t}$ event topology. To see the viability of the proposed technique, we perform Monte Carlo simulations including realistic effects such as cuts, backgrounds, detector resolution, and so on at the LHC of $\sqrt{s}=14$ TeV.Comment: Journal-published version, minor modification in table numbers, 19 pages, 6 figures, 2 tables, references adde

Intra-Abdominal Desmoplastic Small Round Cell Tumor

We report a case of malignant intraabdominal tumor in a 14 years old Korean girl that presented with abdominal pain, distension and palpable mass. Emergency laparotomy revealed bulky peritoneal masses with numerous satellite implanting nodules. Ught microscopically the tumor was characterized by discrete islands of compact, small epithelium-like cells encased in desmoplastic stroma. Immunohistochemically the neoplastic cells expressed vimentin strongly and diffusely and also neuron specific enolase strongly and focally. Ultrastructurally the neoplastic cells showed whorled intermediate filaments, a fair number of mitochondria, dilated rough endoplasmic reticulum, a few fat vacuoles and zonula-adherens type junctions. However there was no evidence of specific differentiation. Histologic, immunohistochemical, and electronmicroscopic observations indicated a primitive malignant neoplasm simultaneously expressing mesenchymal and neural differentiation. Our case did not express any epithelial markers including pancytokeratin, epithelial membrane antigen and CAM 5.2

Protective effect of Buddha’s Temple extract against tert-butyl hydroperoxide stimulation-induced oxidative stress in DF-1 cells

Objective This study aimed to determine the protective efficacy of Buddha’s Temple (BT) extract against tert-butyl hydroperoxide (t-BHP)-induced oxidative stress in Gallus gallus chicken embryo fibroblast cell line (DF-1) and its effects on the cell lipid metabolism. Methods In this experimental study, Gallus gallus DF-1 fibroblast cells were pretreated with BT 10−7 for 24 hours, followed by their six-hour exposure to t-BHP (100 μM). Water-soluble tetrazolium salt-8 (WST-8) assays were performed, and the growth curve was computed. The intracellular gene expression changes caused by BT extract were confirmed through quantitative polymerase chain reaction (qPCR). Flow cytometry, oil red O staining experiment, and thin-layer chromatography were performed for the detection of intracellular metabolic mechanism changes. Results The WST-8 assay results showed that the BT pretreatment of Gallus gallus DF-1 fibroblast cell increased their cell survival rate by 1.08%±0.04%, decreased the reactive oxygen species (ROS) level by 0.93%±0.12% even after exposure to oxidants, and stabilized mitochondrial activity by 1.37%±0.36%. In addition, qPCR results confirmed that the gene expression levels of tumor necrosis factor α (TNFα), TIR domain-containing adapter inducing IFN-beta (TICAM1), and glucose-regulated protein 78 (GRP78) were regulated, which contributed to cell stabilization. Thin-layer chromatography and oil red O analyses showed a clear decrease in the contents of lipid metabolites such as triacylglycerol and free fatty acids. Conclusion In this study, we confirmed that the examined BT extract exerted selective protective effects on Gallus gallus DF-1 fibroblast cells against cell damage caused by t-BHP, which is a strong oxidative inducer. Furthermore, we established that this extract significantly reduced the intracellular ROS accumulation due to oxidative stress, which contributes to an increase in poultry production and higher incomes

Hepatic Ultrastructural Findings of Familial Hyperbilirubinemia Syndrome

Seven liver biopsies of congenital/familial hyperbilirubinemia were studied ultrastructurally including 3 cases of Dubin-Johnson syndrome, 2 cases of Rotor syndrome, one case of Gilbert syndrome and one case of type 2 Crigler-Najjar syndrome. All five cases of Dubin-Johnson syndrome and Rotor's syndrome had conjugated hyperbilirubinemia and both cases of Gilbert's syndrome and a CriglerNajjar syndrome had unconjugated hyperbilirubinemia. In Gilbert's syndrome, the microvilli of the sinusoidal membrane of hepatocytes showed decreased height and number with collagen lay down in the sinusoidal spaces, Megamitochondria, mild proliferation of smooth endoplasmic reticulum, and dilated rough endoplasmic reticulum were also noted. Lipofuscin bodies were seen, but they were less numerous than characteristic Dubin-Johnson bodies. In Crigler-Najjar syndrome, bile canalicular and ductular cholestasis were noted both light microscopically and ultrastructurally. Most bile canaliculi are filled with ovoid homogeneous electron dense material (bile pigments). Widening of the intercellular spaces with increased number of microvilli on the lateral surface of hepatocytes were present. All three cases of Dubin-Johnson syndrome revealed characteristic abundant lysosomal bodies and dilatation of bile canaliculi. These bodies were numerous and membrane bound in round, oval or pleomorphic shapes with variable degrees of electron densities. Dilated bile canaliculi showed expanded lumen with decreased number of microvilli. In Gilbert and Rotor syndromes, the hepatocytes contained lipofuscin-like lysosomal bodies. In both cases of Rotor's syndrome, we found reduced number of microvilli along the sinusoidal side of hepatocyte, like Gilbert syndrome, immature bile canaliculi and pleomorphic megamitochondria and lipofuscin-like lysosomal bodies. We concluded that hepatocytic hyperbilirubinemia syndromes could be differentiated by ultrastructural study along with clinicopathologic correlation

Gamma EEG Correlates of Haptic Preferences for a Dial Interface

Consumers often develop preferences toward consumer electronics based not only on the visual appearance of a product, but also on its haptic interface. If consumers express a strong haptic preference for a consumer electronic product, they are more likely to purchase it. Hence, it is important to understand how consumers' haptic preference for consumer electronics is formed. Conventional paper-based methods may not provide sufficient information for this purpose, because they provide post-event (i.e., after haptic experience) and environment-dependent (i.e., depending on the manner of asking questions, the person asking the questions, and so on.) data. Therefore, the present study investigated haptic preferences for consumer electronics using neural responses during haptic experiences, which provide the advantage of observing changes while the user is manipulating the product and obtaining environment-independent data. We measured neural responses using non-invasive electroencephalography (EEG). Eighteen volunteers participated in the study and manipulated a haptic dial knob that generates four different haptic profiles; during the manipulation, their EEG signals were recorded. After experiencing different haptic profiles, participants reported their level of preference for each profile. The analysis of EEG revealed that frontal gamma oscillations correlate with the level of haptic preferences, with oscillations becoming stronger with increasing haptic preference. The highest correlation between frontal gamma power and haptic preference was found in the early period of the dial task. Therefore, the frontal gamma oscillation of the EEG may represent a neural correlate of the haptic preference and provides a neural basis for understanding this preference in relation to consumer electronics

Perspective of mesenchymal transformation in glioblastoma.

Despite aggressive multimodal treatment, glioblastoma (GBM), a grade IV primary brain tumor, still portends a poor prognosis with a median overall survival of 12-16 months. The complexity of GBM treatment mainly lies in the inter- and intra-tumoral heterogeneity, which largely contributes to the treatment-refractory and recurrent nature of GBM. By paving the road towards the development of personalized medicine for GBM patients, the cancer genome atlas classification scheme of GBM into distinct transcriptional subtypes has been considered an invaluable approach to overcoming this heterogeneity. Among the identified transcriptional subtypes, the mesenchymal subtype has been found associated with more aggressive, invasive, angiogenic, hypoxic, necrotic, inflammatory, and multitherapy-resistant features than other transcriptional subtypes. Accordingly, mesenchymal GBM patients were found to exhibit worse prognosis than other subtypes when patients with high transcriptional heterogeneity were excluded. Furthermore, identification of the master mesenchymal regulators and their downstream signaling pathways has not only increased our understanding of the complex regulatory transcriptional networks of mesenchymal GBM, but also has generated a list of potent inhibitors for clinical trials. Importantly, the mesenchymal transition of GBM has been found to be tightly associated with treatment-induced phenotypic changes in recurrence. Together, these findings indicate that elucidating the governing and plastic transcriptomic natures of mesenchymal GBM is critical in order to develop novel and selective therapeutic strategies that can improve both patient care and clinical outcomes. Thus, the focus of our review will be on the recent advances in the understanding of the transcriptome of mesenchymal GBM and discuss microenvironmental, metabolic, and treatment-related factors as critical components through which the mesenchymal signature may be acquired. We also take into consideration the transcriptomic plasticity of GBM to discuss the future perspectives in employing selective therapeutic strategies against mesenchymal GBM