LazyFrog: Advancing Security and Efficiency in Commercial Wireless Charging with Adaptive Frequency Hopping.

With the proliferation of electronic devices and electricity-based mobility solutions, the significance of wireless power transfer technology has increased substantially. However, ensuring secure and reliable power transmission to authorized users remains a significant challenge. Addressing this complex issue requires an integrated approach that balances efficiency, stability, and security considerations. While current efforts primarily focus on improving charging efficiency and user convenience, integrating robust security measures into wireless charging infrastructure is challenging due to its inherently open nature and susceptibility to external interference. Technical advancements are required to strengthen the security of the wireless charging infrastructure; however, these should be balanced with power loss management. This study tackles two core issues: the increasing hardware requirements for billing system authentication protocols and the interception of wireless charging signals by unauthorized users, leading to power theft and subsequent losses. To address these challenges, we propose a mechanism termed "LazyFrog". This mechanism dynamically adjusts the frequency hopping schedule, activating frequency changes only in response to detected threats during remote charging or upon identifying unauthorized access attempts. The proposed mechanism compares the expected power reception at the device with the actual power supplied by the charging station, enabling the detection of abnormal power losses. By minimizing unnecessary frequency changes and optimizing energy consumption, LazyFrog reduces hardware requirements. Moreover, we have implemented a relative distance estimation mechanism to facilitate efficient power transfer as wireless devices move within the charging environment. With these features, LazyFrog demonstrates a secure, flexible, and energy-efficient wireless charging system ready for practical application.

Protective effects of chebulic acid from Terminalia chebula Retz. against t-BHP-induced oxidative stress by modulations of Nrf2 and its related enzymes in HepG2 cells.

Although chebulic acid isolated from Terminalia chebular has diverse biological effects, its effects on the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and the expression of downstream genes have not been elucidated. The purpose of this research is to investigate the hepatoprotective mechanism of chebulic acid against oxidative stress produced by tert-butyl hydroperoxide (t-BHP) in liver cells. The treatment with chebulic acid attenuated cell death in t-BHP-induced HepG2 liver cells and increased intracellular glutathione content, upregulated the activity of heme oxygenase-1, and also increased the translocation of Nrf2 into the nucleus and Nrf2 target gene expression in a dose-dependent manner. The exposure of chebulic acid activated the phosphorylation of mitogen-activated protein kinases. The overall result is that chebulic acid has cytoprotective effect on t-BHP-induced hepatotoxicity in HepG2 cells through Nrf2-mediated antioxidant enzymes.

A prospective study of temozolomide plus thalidomide during and after radiation therapy for pediatric diffuse pontine gliomas: preliminary results of the Korean Society for Pediatric Neuro-Oncology study.

This prospective study was performed to determine the efficacy and safety of temozolomide (TMZ) plus thalidomide during and after radiation therapy (RT) in pediatric patients with newly diagnosed diffuse pontine glioma (DPG). Seventeen patients with pediatric DPG were enrolled between November 2004 and March 2008. The median age was eight years (range, 3-16 years); seven patients were male and ten were female. With the exception of one glioblastoma case, which was diagnosed via open biopsy, all diagnoses were established using neuroradiological studies. The authors used the Korean Society for Pediatric Neuro-Oncology (KSPNO)-A053 protocol. The mean follow-up period was 12 months (range, 8.5-25 months). Five patients were withdrawn from the study. The rates of response to treatment and survival were analyzed in 12 patients. Ten out of the 12 patients showed a partial response (PR), whereas one patient exhibited stable disease (SD) and another patient had progressive disease (PD). The tumor control rate was 92% (11/12) and the response rate was 83% (10/12). The median progression-free survival (PFS) of the 12 patients was 7.2 months (95% confidence interval (CI), 3.6-10.7). Six-month and twelve-month PFS were 58.3 and 16.7%, respectively. Overall survival (OS) was 12.7 months (95% CI, 10.4-15.1). One and two-year survival were 58.3 and 25%, respectively. The main adverse effect was hematological toxicity, with four patients exhibiting grade 3 or 4 toxicity. All patients tolerated the regimen well enough to continue the adjuvant chemotherapy. No Pneumocystis jiroveci pneumonia was noted. The TMZ plus thalidomide regimen was safe and tolerated well enough to be administered on an outpatient basis. Larger studies are required to demonstrate the efficacy of this regimen.

Phenylbutyrate and phenylacetate induce differentiation and inhibit proliferation of human medulloblastoma cells.

PURPOSE: Phenylbutyrate (PB) and phenylacetate (PA) have antiproliferative and differentiation-inducing effects in malignant tumors, and had been evaluated in Phase I/II clinical trials. This study was undertaken to evaluate their antitumor activities in medulloblastomas. EXPERIMENTAL DESIGN: The biological effects of PB and PA, ranging from 0.1 mM to 3 mM, on two medulloblastoma cell lines (DAOY and D283-MED) were examined using various long-term in vitro and in vivo assays for morphology, proliferation, differentiation, anchorage-independent growth, apoptosis, and tumorigenicity. RESULTS: PB and PA can both induce morphological changes and suppress proliferation in a time- and dose-dependent manner. These effects were more pronounced with PB and became irreversible in D283-MED cells after continuous exposure to 3 mM PB for 28 days. Both PB and PA were able to increase expression of glial marker glial fibriliary acidic protein and neuronal marker synaptophysin in two cell lines. For anchorage-independent growth, PB showed a more significant suppression than PA in D283-MED cells. PB caused more pronounced cell cycle arrest and remarkably reduced tumorigenicity in D283-MED cells than in DAOY cells. Apoptosis was readily induced in D283-MED cells with either low dose of PB or short-term treatment. In contrast, much higher concentrations of PB or longer treatment were required to achieve similar effect with DAOY cells. PB induced increased histones H3 acetylation in both cell lines, but histone H4 acetylation was only observed in D283-MED cells. CONCLUSIONS: PB, through induction of hyperacetylation of histone H3 and H4, is a much more potent antitumor agent than PA. 283-MED cells are more responsive to PB than DAOY cells, which may be dependent on their original state of differentiation as well as the changes of histone H4 acetylation status.

Chemoreduction followed by local therapy and adjuvant chemotherapy for advanced intraocular retinoblastoma: a pilot study in a single center.

Intraocular (IO) retinoblastoma (RB) has traditionally been treated with enucleation (ENU) or external beam radiotherapy (EBRT). Recently, clinical trials are in progress to cure RB without ENU or EBRT in order to salvage the globe and to avoid unacceptable side effects of EBRT. We performed a pilot study to treat patients with advanced Reese-Ellsworth (RE) stage IO RB with initial chemotherapy (CRx) followed by local therapy (LT) and adjuvant CRx. Ten eyes (8 RE group V, 2 RE group IV) from 9 patients were enrolled from March 2001 to November 2001. All tumors responded to CRx. In 5 of 10 eyes, the RB was enough to be treated with LT after chemoreduction. One patient who underwent LT is waiting for ENU due to post-cryotherapy complication. For a median follow-up of 13 months (8-16 mo), 4 eyes that received LT and adjuvant CRx were relapse-free. A patient with bilateral RB who failed to be a candidate for LT was rescued with high-dose CRx and hematopoietic stem cell transplantation. Consequently, by treating patients according to our strategy, we were able to salvage 6 out of 10 eyes without ENU or EBRT. These results suggest that chemoreduction followed by LT and adjuvant CRx might offer the opportunity to salvage the globe and vision even in patients with advanced stage IO RB.

Double high-dose chemotherapy with autologous stem cell transplantation in patients with high-risk neuroblastoma: a pilot study in a single center.

Double high-dose chemotherapy (HDCT) was applied to 18 patients with highrisk neuroblastoma including 14 patients who could not achieve complete response (CR) even after the first HDCT. In 12 patients, successive double HDCT was rescued with peripheral blood stem cells collected during a single round of leukaphereses and in 6 patients, second or more rounds of leukaphereses were necessary after the first HDCT to rescue the second HDCT. The median interval between the first and second HDCT (76 days; range, 47-112) in the single harvest group was shorter than that (274.5 days; range, 83-329) in the double harvest group (p<0.01). Hematologic recovery was slow in the second HDCT. Six (33.3%) treatment-related mortalities (TRM) occurred during the second HDCT but were not related to the shorter interval. Disease-free survival rates at 2 years with a median follow-up of 24 months (range, 6-46) in the single and double harvest group were 57.1% and 33.3%, respectively. These results suggest that successive double HDCT using the single harvest approach may improve the survival of high-risk patients, especially who could not achieve CR after the first HDCT despite delayed hematologic recovery and high rate of TRM during the second HDCT.