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Total annual net primary productions in marine and terrestrial ecosystems are similar. However, a large portion of the newly produced marine phytoplankton biomass is converted to carbon dioxide because of predation. Which food web structure retains high carbon biomass in the plankton community in the global ocean? In 6954 individual samples or locations containing phytoplankton, unicellular protozooplankton, and multicellular metazooplankton in the global ocean, phytoplankton-dominated bottom-heavy pyramids held higher carbon biomass than protozooplankton-dominated middle-heavy diamonds or metazooplankton-dominated top-heavy inverted pyramids. Bottom-heavy pyramids predominated, but the high predation impact by protozooplankton on phytoplankton or the vertical migration of metazooplankton temporarily changed bottom-heavy pyramids to middle-heavy diamonds or top-heavy inverted pyramids but returned to bottom-heavy pyramids shortly. This finding has profound implications for carbon retention by plankton communities in the global ocean.
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Cadena Alimentaria , Plancton , Ecosistema , Biomasa , Fitoplancton , DiamanteRESUMEN
Gastric cancer stem-like cells (GCSCs) possess stem cell properties, such as self-renewal and tumorigenicity, which are known to induce high chemoresistance and metastasis. These characteristics of GCSCs are further enhanced by autophagy, worsening the prognosis of patients. Currently, the mechanisms involved in the induction of stemness in GCSCs during autophagy remain unclear. In this study, we compared the cellular responses of GCSCs with those of gastric cancer intestinal cells (GCICs) whose stemness is not induced by autophagy. In response to glucose starvation, the levels of ß-catenin and stemness-related genes were upregulated in GCSCs, while the levels of ß-catenin declined in GCICs. The pattern of deubiquitinase ubiquitin C-terminal hydrolase-L3 (UCH-L3) expression in GCSCs and GCICs was similar to that of ß-catenin expression depending on glucose deprivation. We also observed that inhibition of UCH-L3 activity reduced ß-catenin protein levels. The interaction between UCH-L3 and ß-catenin proteins was confirmed, and it reduced the ubiquitination of ß-catenin. Our results suggest that UCH-L3 induces the stabilization of ß-catenin, which is required to promote stemness during autophagy activation. Also, UCH-L3 expression was regulated by c-Fos, and the levels of c-Fos increased in response to autophagy activation. In summary, our findings suggest that the inhibition of UCH-L3 during nutrient deprivation could suppress stress resistance of GCSCs and increase the survival rates of gastric cancer patients.
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Neoplasias Gástricas , Humanos , Neoplasias Gástricas/genética , beta Catenina/metabolismo , Células Madre Neoplásicas/metabolismo , UbiquitinaciónRESUMEN
High thermal stability is crucial for the commercialization of organic solar cells (OSCs). The thermal stability of OSCs has been improved using the tailoring blend morphology of bulk heterojunctions (BHJs). Herein, we demonstrated thermally stable OSCs in a ternary blended system containing low-crystalline semiconducting polymers (asy-PNDI1FTVT and PTB7-Th) and a non-fullerene acceptor (Y6). The asymmetric n-type semiconducting polymer (asy-PNDI1FTVT) differed from general symmetric semiconducting polymers as it randomly substituted fluorine atoms at the donor moiety (TVT), resulting in significantly lower crystallinity. asy-PNDI1FTVT in PTB7-Th:Y6 exhibited a well-mixed morphology at the BHJ and efficiently facilitated the charge dissociation process with an enhanced fill factor and power conversion efficiency. Furthermore, the ternary system of PTB7-Th:Y6:asy-PNDI1FTVT suppressed phase separation with negligible burn-in loss and performance degradation under thermal stress. The experiments showed that our devices without encapsulation retained over 90% of their initial efficiencies after 100 h at 65 °C. These results show significant potential for the development of thermally stable OSCs with reasonable efficiency.
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T-LAK cell originated protein kinase (TOPK) has been shown to regulate proliferation, invasion or migration of various cancer cells. However, the role of TOPK in follicle environments remains unknown. Here we reveal that TOPK inhibits TNF-α-induced human granulosa COV434 cell apoptosis. The expression of TOPK were increased in COV434 cells in response to TNF-α. TOPK inhibition also decreased TNF-α-induced SIRT1 expression but promoted TNF-α-induced p53 acetylation and expression of PUMA or NOXA. Accordingly, TOPK inhibition attenuated TNF-α-mediated SIRT1 transcriptional activity. In addition, SIRT1 inhibition augmented acetylation of p53 or expression of PUMA and NOXA in response to TNF-α, leading to COV434 cell apoptosis. We conclude that TOPK suppresses TNF-α-induced COV434 granulosa cell apoptosis via regulation of p53/SIRT1 axis, suggesting a potential role of TOPK in regulation of ovarian follicular development.
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Apoptosis , Células de la Granulosa , Factor de Necrosis Tumoral alfa , Proteína p53 Supresora de Tumor , Femenino , Humanos , Apoptosis/fisiología , Proteínas Reguladoras de la Apoptosis/metabolismo , Quinasas MAP Reguladas por Señal Extracelular/metabolismo , Células de la Granulosa/metabolismo , Quinasas de Proteína Quinasa Activadas por Mitógenos/metabolismo , Sirtuina 1/genética , Sirtuina 1/metabolismo , Factor de Necrosis Tumoral alfa/farmacología , Factor de Necrosis Tumoral alfa/metabolismo , Proteína p53 Supresora de Tumor/metabolismoRESUMEN
Organic photovoltaics (OPVs) have emerged as a promising next-generation technology with great potential for portable, wearable, and transparent photovoltaic applications. Over the past few decades, remarkable advances have been made in non-fullerene acceptor (NFA)-based OPVs, with their power conversion efficiency exceeding 18%, which is close to the requirements for commercial realization. Novel molecular NFA designs have emerged and evolved in the progress of understanding the physical features of NFA-based OPVs in relation to their high performance, while there is room for further improvement. In this review, the molecular design of representative NFAs is described, and their blend characteristics are assessed via statistical comparisons. Meanwhile, the current understanding of photocurrent generation is reviewed along with the significant physical features observed in high-performance NFA-based OPVs, while the challenging issues and the strategic perspectives for the commercialization of OPV technology are also discussed.
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Microalgae fuel food webs and biogeochemical cycles of key elements in the ocean. What determines microalgal dominance in the ocean is a long-standing question. Red tide distribution data (spanning 1990 to 2019) show that mixotrophic dinoflagellates, capable of photosynthesis and predation together, were responsible for ~40% of the species forming red tides globally. Counterintuitively, the species with low or moderate growth rates but diverse prey including diatoms caused red tides globally. The ability of these dinoflagellates to trade off growth for prey diversity is another genetic factor critical to formation of red tides across diverse ocean conditions. This finding has profound implications for explaining the global dominance of particular microalgae, their key eco-evolutionary strategy, and prediction of harmful red tide outbreaks.
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A small dinoflagellate, ~13 µm in cell length, was isolated from Jinhae Bay, Korea. Light microscopy showed that it was similar to the kleptoplastidic dinoflagellate Gymnodinium gracilentum nom. inval. rDNA sequences were obtained and its anatomy and morphology described using light and scanning and transmission electron microscopy. Phylogenetic analyses indicated that it belonged to the family Kareniaceae. However, its large subunit (LSU) rDNA sequences were 5.2-9.5% different from those of the other five genera in the family, and its clade was clearly divergent from that of each genus. Its overall morphology was different from those of the other five genera in the family and from Gymnodinium. Unlike Gymnodinium, this dinoflagellate did not have a horseshoe-shaped apical groove, nuclear envelope chambers, or a nuclear fibrous connective (NFC). It had an apical line of narrow amphiesmal vesicles and an elongated apical furrow crossing the apex. Cells were covered with polygonal amphiesmal vesicles arranged in 16 rows. Starved cells did not contain their own plastids, eyespots, pyrenoids, peridinin, or fucoxanthin. However, they could survive without added prey for approximately one month using chloroplasts from the cryptophyte prey Teleaulax amphioxeia, indicating kleptoplastidy. Because this taxon is genetically distinct at the generic rank from the other genera in Kareniaceae, it is placed in Shimiella gen. nov., and because G. gracilentum was invalid, the new bionomial S. gracilenta sp. nov. is proposed.
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Dinoflagelados , ADN Protozoario , ADN Ribosómico , Dinoflagelados/genética , Filogenia , República de CoreaRESUMEN
Oxidative stress has been suggested to induce granulosa cell apoptosis, which contributes to follicular atresia. However, the mechanism via which oxidative stress mediates granulosa cell apoptosis remains elusive. Therefore, the aim of this study was to elucidate the molecular mechanisms regulating oxidative stressinduced granulosa cell apoptosis. The present study demonstrated that reactive oxygen species induced by H2O2 resulted in human granulosa COV434 cell apoptosis via the regulation of sirtuin 1 (SIRT1)mediated p53 activity. Endogenous SIRT1 expression was alleviated by H2O2 treatment of COV434 cells in a timedependent manner. In addition, knockdown or inhibition of SIRT1 promoted H2O2induced poly(ADPribose) polymerase (PARP) cleavage and p53 acetylation, which led to an increase in COV434 cell apoptosis. Treatment with H2O2 enhanced the expression levels of the p53dependent proteins, p53upregulated modulator of apoptosis (PUMA) and phorbol12myristate13acetateinduced protein 1 (PMAIP1), as well as those of p53; however, knockdown of p53 decreased cleaved PARP, PUMA and PMAIP1 expression levels induced by H2O2 treatment. Moreover, knockdown of PUMA or PMAIP1 attenuated the H2O2 induction of PARP cleavage and COV434 cell apoptosis. In conclusion, the present findings suggested that H2O2induced oxidative stress causes granulosa COV434 cell apoptosis via the upregulation of p53 activity by SIRT1 suppression, indicating a mechanistic role of the SIRT1/p53 axis in H2O2induced granulosa cell apoptosis.
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Células de la Granulosa/citología , Peróxido de Hidrógeno/efectos adversos , Sirtuina 1/metabolismo , Proteína p53 Supresora de Tumor/metabolismo , Apoptosis , Regulación hacia Abajo , Femenino , Regulación de la Expresión Génica/efectos de los fármacos , Técnicas de Silenciamiento del Gen , Células de la Granulosa/efectos de los fármacos , Células de la Granulosa/metabolismo , Humanos , Estrés Oxidativo , Especies Reactivas de Oxígeno/metabolismo , Sirtuina 1/genética , Factores de Tiempo , Regulación hacia ArribaRESUMEN
It has been suggested that oxidative stress involving reactive oxygen species (ROS) induces granulosa cell apoptosis, leading to follicular atresia, and that Tlymphokineactivated killer celloriginated protein kinase (TOPK) suppresses cancer cell apoptosis induced by several stimuli. However, it remains to be determined whether TOPK affects oxidative stressinduced granulosa cell apoptosis. The present study demonstrates that TOPK inhibition increases human granulosa COV434 cell apoptosis induced by hydrogen peroxide (H2O2). Cotreatment with the TOPK inhibitor, OTS514, in combination with H2O2 increased p53 acetylation and its expression, whereas it decreased Sirtuin 1 (SIRT1) expression, contributing to the promotion of apoptosis. In addition, the SIRT1 activator, resveratrol, or the SIRT1 inhibitor, Ex527, reduced or elevated H2O2induced COV434 cell apoptosis, respectively. Furthermore, the p53 inhibitor, Pifithrinµ, diminished the augmentation in poly(ADPribose) polymerase (PARP) cleavage induced by OTS514 plus H2O2, while the Mdm2 antagonist, Nutlin 3, increased PARP cleavage. Moreover, OTS514 further decreased the SIRT1 transcriptional activity decreased by H2O2, but promoted the H2O2induced p53 or p21 transcriptional activity. Notably, the expression of exogenous p53 reduced SIRT1 transcriptional activity. Taken together, the findings of the present study demonstrate that TOPK inhibition promotes p53mediated granulosa cell apoptosis through SIRT1 downregulation in response to H2O2. Therefore, it can be concluded that TOPK suppresses H2O2induced apoptosis through the modulation of the p53/SIRT1 axis, suggesting a potential role of TOPK in the regulation of human granulosa cell apoptosis, leading to the promotion of abnormal follicular development.
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Apoptosis/efectos de los fármacos , Células de la Granulosa/efectos de los fármacos , Quinasas de Proteína Quinasa Activadas por Mitógenos/antagonistas & inhibidores , Quinasas de Proteína Quinasa Activadas por Mitógenos/metabolismo , Estrés Oxidativo/efectos de los fármacos , Sirtuina 1/metabolismo , Proteína p53 Supresora de Tumor/metabolismo , Acetilación/efectos de los fármacos , Apoptosis/genética , Línea Celular Tumoral , Regulación hacia Abajo/efectos de los fármacos , Femenino , Atresia Folicular/efectos de los fármacos , Atresia Folicular/metabolismo , Células de la Granulosa/metabolismo , Células de la Granulosa/patología , Humanos , Peróxido de Hidrógeno/farmacología , Poli(ADP-Ribosa) Polimerasas/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Transcripción Genética/efectos de los fármacosRESUMEN
PDZ-binding kinase (PBK) has previously been shown to mediate chemoresistance of cancer cells to anticancer drugs. However, it remains unclear how PBK regulates paclitaxel-induced cancer cell death. Here, we demonstrate that PBK hinders paclitaxel-mediated autophagic cell death in H460 non-small-cell lung cancer cells. PBK knockdown increased apoptosis, autophagy, p53 level, and LC3 puncta upon paclitaxel treatment. Moreover, p53 expression facilitated an increase in the LC3-II/LC3-I ratio in response to paclitaxel, and PBK knockdown augmented paclitaxel-mediated p53 transcriptional activity. Meanwhile, paclitaxel induced PBK-mediated p53 nuclear export and its subsequent ubiquitination in control cells, but not in PBK knockdown cells. We conclude that PBK hampers paclitaxel-induced autophagic cell death by suppressing p53, suggesting a potential role of PBK in p53-mediated H460 cell death.
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Carcinoma de Pulmón de Células no Pequeñas/metabolismo , Quinasas de Proteína Quinasa Activadas por Mitógenos/metabolismo , Antineoplásicos/farmacología , Apoptosis/efectos de los fármacos , Muerte Celular Autofágica/efectos de los fármacos , Autofagia/efectos de los fármacos , Carcinoma de Pulmón de Células no Pequeñas/genética , Línea Celular Tumoral , Supervivencia Celular/efectos de los fármacos , Expresión Génica/genética , Regulación Neoplásica de la Expresión Génica/genética , Humanos , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/metabolismo , Paclitaxel/metabolismo , Paclitaxel/farmacología , Proteína p53 Supresora de Tumor/efectos de los fármacos , Proteína p53 Supresora de Tumor/metabolismoRESUMEN
For emerging biocompatible, wearable, and stretchable epidermal electronic devices, it is essential to realize novel stretchable conductors with the attributes of transparency, low-cost and nontoxic components, green-solvent processbility, self-healing, and thermal stabililty. Although conducting materials-rubber composites, ionic hydrogels, organogels have been developed, no stretchable material system that meets all the outlined requirements has been reported. Here, a series of P(SPMA-r-MMA) polymers with different ratios of ionic side chains is designed and synthesized, and it is demonstrated that the resulting stretchable ionic conductors with glycerol are transparent, water processable, self-healable, and thermally stable due to the chemically linked ionic side chain, satisfying all of the aforementioned requirements. Among the series of polymer gels, the P(SPMA0.75 -r-MMA0.25 ) gel shows optimum conductivity (6.7 × 10-4 S cm-1 ), stretchability (2636% of break at elongation), and self-healing (98.3% in 3 h) properties. Accordingly, the transparent and self-healable P(SPMA0.75 -r-MMA0.25 ) gels are used to realize thermally robust actuators up to 100 °C and deformable and self-healable thermal sensors.
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Numerous previous studies have focused on the notion that semiconducting polymers with an edge-on dominant orientation are advantageous for horizontal charge transport, whereas polymers with a face-on dominant orientation are advantageous for vertical charge transport, since the crystallite orientation determines the π-π stacking direction, which in turn affects the interchain charge transport direction. Here, we report that the crystallite orientation is dependent on the intermolecular interactions in the semiconducting polymer. In this study, we control the intermolecular interactions in a donor-acceptor (D-A) semiconducting polymer via side chain engineering. To perform side chain engineering, we use two different polymers: one with side chains on only A units (PDPP-B) and the other with side chains on both D and A units (PDPP-C8). We observe that PDPP-C8 is characterized by weaker intermolecular interactions due to the additional side chains on D units. A morphological analysis reveals that PDPP-B and PDPP-C8 films have microstructures that are characterized by edge-on and face-on dominant orientations, respectively. Therefore, we demonstrate that our strategies effectively control intermolecular interactions and, consequently, the crystallite orientation. Finally, we compare the vertical and horizontal mobilities of both polymer films. These results show that the crystallite orientation has significant influence on charge transport behaviors.