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Solar energy has gained prominence because of the increasing global attention received by renewable energies. This shift can be attributed to advancements and innovations in solar cell technology, which include developments of various photovoltaic materials, such as thin film and tandem solar cells, in addition to silicon-based solar cells. The latter is the most widely commercialized type of solar cell because of its exceptional durability, long-term stability, and high photoconversion efficiency; consequently, the demand for Si solar cells has been consistently increasing. PV modules are designed for an operation lifespan of 25–30 years, which has led to a gradual increase in the number of end-of-life PV modules. The appropriate management of both end-of-life and prematurely failed PV modules is critical for the recovery and separation of valuable and hazardous materials. Effective methods for end-of-life PV waste management are necessary to minimize their environmental impact and facilitate transition to a more sustainable and circular economy. This paper offers a comprehensive overview of the separation processes for silicon PV modules and summarizes the attempts to design easily recyclable modules for sustainable solar module development. Based on the studies summarized in this paper, suggestions are provided for future research.

The guaianolide family of sesquiterpene lactones is known for its distinctive structural features and diverse biological activities. 4,9,10-Trihydroxyguaia-11(13)­en-12,6-olide, with an underdetermined absolute stereochemistry (1 or ent-1), is a newly identified 6,12-guaianolide isolated from the genus Anvillea garcinii. Motivated by the potential biological activity of the natural product, we pursue its stereoselective synthesis. Starting from (R)-limonene, an asymmetric total synthesis of 4α,9α,10α-trihydroxyguaia-11(13)­en-12,6α-olide (1) is accomplished in 20 steps with an overall yield of 4%, utilizing key transformations such as stereoselective reductive epoxide opening and additions of methyl lithiopropiolate and allyl cuprate. Most significantly, preliminary biological testing uncovers new anticancer activity of 1 against rare and aggressive childhood atypical teratoid rhabdoid tumor (ATRT) and other cancer cell lines. We anticipate that our synthetic strategy will enable the development of chemical probes and derivatives derived from 1 for mechanism of action studies and anticancer drug discovery.

The aim of this study is to quantitatively compare the field performance of two bifacial photovoltaic (PV) technologies—Passivated Emitter and Rear Contact (PERC) and Tunnel Oxide Passivated Contact (TOPCon)—under real‐world rooftop conditions in winter in South Korea. PV module efficiency obtained under standard test conditions, such values can diverge significantly from actual field performance, directly impacting energy yield and the levelized cost of energy. This study employed a 20‐day rooftop field test on a south‐facing building to evaluate and compare the energy yield and electrical characteristics of PERC and TOPCon modules. TOPCon achieved an 8.16% higher energy yield than PERC, owing to its higher bifaciality coefficient (83.3% vs. 78.8%), better temperature coefficient of voltage, and lower rear‐side shading. TOPCon thus achieved 1.51% higher normalized open‐circuit voltage (Voc) and 7.40% higher normalized short‐circuit current (Isc). This study, the first to decompose the normalized Voc and Isc contributions under field conditions, confirms that device‐level innovations in cell architecture can substantially improve real‐world energy generation. These findings underscore the importance of optimizing module design based on field conditions rather than relying solely on laboratory benchmarks. We fabricated modules using Tunnel Oxide Passivated Contact and Passivated Emitter and Rear Contact solar cells, installed them outdoors, and compared their energy yields. This paper examines the factors contributing to the differences in energy yield, considering everything from the manufacturing processes of each solar cell to their electrical parameters (Voc, Isc, QE) and outdoor environmental conditions.

Trinucleotide repeat instability has been implicated in the pathogenesis of numerous neurodegenerative disorders. While germline expansions destabilize trinucleotide repeats to cause disease anticipation, somatic cell trinucleotide repeat instability drives earlier onset of symptoms and further disease progression. However, the drivers behind these repeat length changes remain unclear. Current models suggest that DNA replication slippage events and the action of genome instability pathways, such as DNA repair, cause trinucleotide repeat mutagenesis. Whether mutagenic polymerases from the translesion synthesis pathway result in trinucleotide repeat instability is unclear. Translesion synthesis polymerases are best at bypassing difficult-to-replicate DNA regions due to bulky lesions or gaps in DNA. While some effects of translesion synthesis polymerases on trinucleotide repeat instability have been explored in lower organisms, evidence in human cells is lacking. Using a quantitative green fluorescent protein (GFP) reporter with expanded CAG repeats, we show that inhibition of the translesion synthesis polymerase REV1 by its inhibitor, JH-RE-06, or siRNA knockdown increases trinucleotide repeat instability and the underlying mutability. These results suggest that REV1 protects trinucleotide repeat length mutagenesis through potential continuous DNA synthesis when replicative polymerases stall ahead of repeat secondary structures. Collectively, we present evidence of the translesion synthesis pathway’s role in trinucleotide repeat instability, with potential implications for understanding mutability mechanisms, disease biology and therapeutic targeting.

Photovoltaic (PV) installations have traditionally relied on a conventional south-facing orientation, which maximizes energy production at noon but has lower energy generation in the morning and afternoon. Vertical photovoltaic (VPV) systems have emerged as promising alternatives to address this inconsistency. Vertical photovoltaic systems can enhance energy generation by facing east in the morning and west in the afternoon. We compared the performance of n-tunnel oxide passivated contact (n-TOPCon) and p-passivated emitter and rear contact (p-PERC) cells in vertical photovoltaic systems to determine whether the optimal installation direction of bifacial vertical photovoltaics is east or west. Our findings indicated that n-TOPCon cells exhibited higher energy yields than p-PERC cells, with a difference of approximately 8%, attributed to the superior bifaciality and lower temperature coefficient of power of n-TOPCon. Additionally, the energy yield was higher for n-TOPCon modules when the front faced east, whereas the PERC modules performed better with a west-facing front. This contributes to the knowledge of the factors for energy production in vertical photovoltaic systems and the optimization of installation configurations.

Reverse Nearest Neighbor (RNN) query is to find the set of objects that are closer to the Q than any other objects in dataset D. Owing to the wide application spectrum, there have been great demands for effective RNN query processing in the circumstance where the sensor nodes are deployed over a wide geographical area and track the location of objects. However, relentless energy and computing resource depletion are inevitable by the maintaining the infrastructures in the existing researches. Motivated by these issues, we propose a novel approach, named the parallel itinerary-based RNN (PIRNN) query processing algorithm which does not rely on any kind of infrastructures. PIRNN disseminates multiple itineraries concurrently and it prunes the search area to increase performance. Furthermore, we extend PIRNN with two optimization heuristics, called Peri-Segment Completion (PSC) and Look Forward (LF) to minimize the area to be searched. In order to evaluate the performance of PIRNN query processing, we compare PIRNN with itinerary-based SAA and TPL. The extensive simulation results show that the PIRNN method outperforms SAA and TPL in terms of network traffic.

Trinucleotide repeat (TNR) instability has been implicated in the pathogenesis of numerous neurodegenerative disorders. Because TNR instability causes mutagenesis of the underlying gene, we refer to the repeat instability phenomenon as TNR mutagenesis in this study. While germline expansions destabilize TNR to cause disease anticipation, somatic cell TNR instability drives earlier onset of symptoms and further disease progression. However, the drivers behind these repeat length changes remain unclear. Current models suggest that DNA replication slippage events and the action of genome instability pathways, such as DNA repair, cause TNR mutagenesis. Whether mutagenic polymerases from the translesion synthesis (TLS) pathway result in TNR instability is unclear. TLS polymerases are best at bypassing difficult-to-replicate DNA regions due to bulky lesions or gaps in DNA. While some effects of TLS polymerases on TNR instability have been explored in lower organisms, evidence in human cells is lacking. Using a quantitative GFP reporter with expanded CAG repeats, we show that inhibition of the TLS polymerase REV1 by its inhibitor, JH-RE-06, or siRNA knockdown increases TNR instability and the underlying mutability. These results suggest that REV1 protects Trinucleotide repeat length mutagenesis through potential continuous DNA synthesis when replicative polymerases stall ahead of repeat secondary structures. Collectively, we present evidence of the role of the TLS pathway in TNR instability, with potential implications for understanding mutability mechanisms, disease biology, and therapeutic targeting.

Invasive fungal infections are a leading cause of death worldwide. Translating molecular insights into clinical benefits is challenging because fungal pathogens and their hosts share similar eukaryotic physiology. Consequently, current antifungal treatments have limited efficacy, may be poorly fungicidal in the host, can exhibit toxicity, and are increasingly compromised by emerging resistance. We have established that the phosphatase calcineurin (CaN) is required for invasive fungal disease and an attractive target for antifungal drug development. CaN is a druggable target, and there is vast clinical experience with the CaN inhibitors FK506 and cyclosporin A (CsA). However, while FK506 and its natural analog FK520 exhibit antifungal activity, they are also immunosuppressive in the host and thus not fungal-selective. We leverage our pathogenic fungal CaN-FK506-FKBP12 complex X-ray structures and biophysical data to support structure-based ligand design as well as structure-activity relationship analyses of broad-spectrum FK506/FK520 derivatives with potent antifungal activity and reduced immunosuppressive activity. Here we apply molecular docking studies to develop antifungal C22- or C32-modified FK520 derivatives with improved therapeutic index scores. Among them, the C32-modified FK520 derivative JH-FK-44 ( ) demonstrates a significantly improved therapeutic index compared to JH-FK-08, our lead compound to date. NMR binding studies with C32-derivatives are consistent with our hypothesis that C32 modifications disrupt the hydrogen bonding network in the human complex while introducing favorable electrostatic and cation-π interactions with the fungal FKBP12 R86 residue. These findings further reinforce calcineurin inhibition as a promising strategy for antifungal therapy. Invasive fungal infections cause significant mortality worldwide, and current antifungal treatments are often ineffective, toxic, or face growing resistance. This research identifies calcineurin (CaN), a critical protein for fungal survival, as a potential target for developing new antifungal drugs. Although existing CaN inhibitors such as FK506 (tacrolimus) and FK520 (ascomycin) possess antifungal properties, their immunosuppressive effects limit their clinical utility. By studying the structure of human and fungal FKBP12-FK506 or FK520 complexes with CaN, we have designed and synthesized modified FK520 derivatives with strong antifungal activity and reduced immunosuppressive effects. These new derivatives are expected to have significantly improved therapeutic profiles, offering hope for more effective and safer antifungal treatments.

Standard initial systemic treatment for patients with metastatic prostate cancer includes agents that target androgen receptor (AR) signaling. Despite an initial positive response to these AR pathway inhibitors (ARPIs), acquired resistance remains a significant challenge. We show that treatment of AR-positive prostate cancer cells with the frontline ARPI enzalutamide induces DNA replication stress. Such stress is exacerbated by suppression of translesion DNA synthesis (TLS), leading to aberrant accumulation of single-stranded DNA (ssDNA) gaps and persistent DNA damage biomarkers. We further demonstrate that the TLS inhibitor, JH-RE-06, markedly sensitizes AR-positive prostate cancer cells, but not AR-negative benign cells, to enzalutamide Combination therapy with enzalutamide and JH-RE-06 significantly suppresses cancer growth in a syngeneic murine tumor model over vehicle control or individual treatment groups. These findings suggest that AR inhibition broadly triggers DNA replication stress in hormone-sensitive prostate cancer, thereby exposing a unique vulnerability that can be exploited by a TLS-disrupting adjuvant for targeted therapy.

Invasive fungal infections are a leading cause of death worldwide. Translating molecular insights into clinical benefits is challenging because fungal pathogens and their hosts share similar eukaryotic physiology. Consequently, current antifungal treatments have limited efficacy, may be poorly fungicidal in the host, can exhibit toxicity, and are increasingly compromised by emerging resistance. We have established that the phosphatase calcineurin (CaN) is required for invasive fungal disease and an attractive target for antifungal drug development. CaN is a druggable target, and there is vast clinical experience with the CaN inhibitors FK506 and cyclosporin A (CsA). However, while FK506 and its natural analog FK520 exhibit antifungal activity, they are also immunosuppressive in the host and thus not fungal-selective. We leverage our pathogenic fungal CaN-FK506-FKBP12 complex X-ray structures and biophysical data to support structure-based ligand design as well as structure–activity relationship analyses of broad-spectrum FK506/FK520 derivatives with potent antifungal activity and reduced immunosuppressive activity. Here we apply molecular docking studies to develop antifungal C22- or C32-modified FK520 derivatives with improved therapeutic index scores. Among them, the C32-modified FK520 derivative JH-FK-44 ( 7 ) demonstrates a significantly improved therapeutic index compared to JH-FK-08, our lead compound to date. NMR binding studies with C32-derivatives are consistent with our hypothesis that C32 modifications disrupt the hydrogen bonding network in the human complex while introducing favorable electrostatic and cation–π interactions with the fungal FKBP12 R86 residue. These findings further reinforce calcineurin inhibition as a promising strategy for antifungal therapy.