Browsing by Author "Chang, Hsin-Yun"

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A Piezoceramic Sensor for Detection of Focused Ultrasound-Induced Cavitation
(2019-11-15)
Chen, Jung-Chih
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Chang, Hsin-Yun
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Chen, Jiun-Jung
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Chen, Gin-Shin
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分子醫學與生物工程研究所
Acoustic cavitation plays a key role in blood-brain-barrier opening. Stable cavitation is required for safely transient barrier disruption when inertial cavitation may cause potentially undesirable damage to brain. To ensure the safety, an appropriate passive cavitation detector is needed to monitor cavitation activity during focused ultrasound treatment. The purpose of this study was to develop a passive cavitation detector with high sensitivity at the specific frequency used in blood-brain-barrier opening. The detector was designed with the assistance of pulse-echo response simulations, using the software PiezoCAD. The active transducer of the detector was constructed of two matching layers, a PZT-5A ceramic disk and the titanium backing. The detector was characterized via the pulse-echo measurements and a commercial hydrophone was used to determine the sensitivity of the developed detector. Cavitation experiments were also performed to validate the detector. The experimental results showed that the detector had the center frequency of 1.16 MHz with the bandwidth of 44.8% and its sensitivity was 2.87 V / MPa at 1.0 MHz. In cavitation experiments, 2-MHz focused ultrasound with the focal intensity of 58 W/cm(2) and 1461 W/cm(2) induced stable cavitation and inertial cavitation in free field, separately. The spectra of the ultrasound signals detected by the detector indicated the occurrence of peak voltages at the subharmonic frequency of 1 MHz and the increase in the level of wideband signals, reflecting stable cavitation and inertial cavitation, respectively. Based on the design guideline of this study, the passive cavitation detector can be developed dedicated for blood-brain-barrier opening.
Fault-tolerance and Minimum Cost Placement of Bistatic Radar Sensors forBelt Barrier Coverage
(2016-01-01)
Chang, Hsin-Yun
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Kao, Louis
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Chang, Kai-Po
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Chen, Chiuyuan
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應用數學系
Barrier coverage is an important problem in wireless sensor networks and is used to guarantee the detection of an intruder that tries to cross a protected region. Most of previous studies on barrier coverage are based on the disk coverage model or sector coverage model. Recently, barrier coverage based on the bistatic radar sensor model has received more attention. The coverage area of abistatic radar is different from that of the disk and sector coverage and is dependent on the distance between the transmitter and the receiver. In particular, in [8], Wang et al. studied belt barrier coverage in bistatic radar sensor model and proposed algorithms that minimize the total placement cost spent in constructing the barrier. Note that belt barrier is a line barrier with the breadth not smaller than a predefined threshold so that the coverage quality can be improved. The purpose of this paper is to study belt barrier coverage in bistatic radar sensor model. We first propose a new deployment method that further reduces the total placement cost of [8]. We then study the fault-tolerance issue and the energy-saving issue. To the best of our knowledge, our work is the first paper that studies these two issues in belt barrier coverage in bistatic radar sensor model.
Multiple Functions of KBP in Neural Development Underlie Brain Anomalies in Goldberg-Shprintzen Syndrome
(2019-11-01)
Chang, Hsin-Yun
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Cheng, Haw-Yuan
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Tsao, Ai-Ni
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Liu, Chen
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Tsai, Jin-Wu
Kinesin-binding protein (KBP; KIF1BP; KIAA1279) functions as a regulator for a subset of kinesins, many of which play important roles in neural development. Previous studies have shown that KBP is expressed in nearly all tissue with cytoplasmic localization. Autosomal recessive mutations in KIAA1279 cause a rare neurological disorder, Goldberg-Shprintzen syndrome (GOSHS), characterized by microcephaly, polymicrogyria, intellectual disability, axonal neuropathy, thin corpus callosum and peripheral neuropathy. Most KIAA1279 mutations found in GOSHS patients are homozygous nonsense mutations that result in KBP loss-of-function. However, it is not fully understood how KBP dysfunction causes these defects. Here, we used in utero electroporation (IUE) to express KBP short hairpin RNA (shRNA) with green fluorescent protein (GFP) in neural progenitor cells of embryonic day (E) 14 mice, and collected brain slices at different developmental stages. By immunostaining of neuronal lineage markers, we found that KBP knockdown does not affect the neural differentiation process. However, at 4 days post IUE, many cells were located in the intermediate zone (IZ). Moreover, at postnatal day (P) 6, about one third of the cells, which have become mature neurons, remained ectopically in the white matter (WM), while cells that have reached Layer II/III of the cortex showed impaired dendritic outgrowth and axonal projection. We also found that KBP knockdown induces apoptosis during the postnatal period. Our findings indicate that loss of KBP function leads to defects in neuronal migration, morphogenesis, maturation, and survival, which may be responsible for brain phenotypes observed in GOSHS.