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Liljeblad, Jonathan. "China, western art museums, and dissident art via social networks." Poster 3, no. 1 (December 1, 2015): 7–18. http://dx.doi.org/10.1386/post.3.1-2.7_1.
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Munir, Fakhr ul, Nelofar Ihsan, and Sanaullah. "Strategic and Economic Importance of Gwadar for China and other Regional and Western States." Global Economics Review VI, no. III (September 30, 2021): 22–30. http://dx.doi.org/10.31703/ger.2021(vi-iii).03.
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Gwadar is a deep seaport that played the role of main communication and trade route among India and the Gulf States. In collaboration with China, Gwadar Port has been intended to be connected with Afghanistan and via Afghanistan to Central Asia through road links. If we take the case of the Arabian Sea and the Indian Ocean, it is Gwadar Port that allows China to counterbalance the Indo-US supremacy. Beijing now has the ability to counterbalance Indian maritime activities in the Indian Ocean by praising and acknowledging this Port. Gwadar Port's distance from Pakistan's Karachi Port and India's Gujarat and Mumbai naval stations allows China to observe Indo-US naval operations in the Indian Ocean and the Persian Gulf. Persia Gulf is responsible for over 60% of Beijing's energy supply demands. This phenomenon, in the long run, allows Beijing to monitor and control the sea lanes of communication (SLOCs) from the Persian Gulf to the Indian Ocean and up to the Strait of Hormuz.
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Scott, John K., and Kathryn L. Batchelor. "Management of Chrysanthemoides monilifera subsp. rotundata in Western Australia." Invasive Plant Science and Management 7, no. 1 (March 2014): 190–96. http://dx.doi.org/10.1614/ipsm-d-13-00052.1.
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AbstractOne of Australia's most serious weeds, Chrysanthemoides monilifera subsp. rotundata (bitou bush) was recently found for the first time in Western Australia as a well established population in Kwinana, a major port and industrial area south of Perth, the State's capital. This population is remote from other bitou bush infestations in Australia and had escaped detection despite extensive surveys in the same State for the other subspecies that is present in Australia, Chrysanthemoides monilifera subsp. monilifera (boneseed). The main reasons it went undetected are thought to be the tightly controlled access to this area because of mineral processing and port activities, the unusual invasion route via a heavy industrial area and the morphological similarity to a native species when it is not flowering. Two surveys defined the core population of 1038 plants that are spread along the coast over a 25-ha semi-circle with about a 500-m (1640 ft) diameter. Subsequent surveys of first a 500 m buffer zone and later a 1-km (0.621 mi) buffer found four additional plants, indicating that there is considerable potential for dispersal. We concluded that the survey has not delimited the distribution because of the potential and evidence for long distance dispersal. Cooperation by the various land managers has led to all plants being killed, as an initial step to management of this species. Other steps to be undertaken include an awareness campaign in the area that would need to be surveyed for delimitation of the spatial distribution and seed bank assessment to measure potential dispersal both in space and through time. It remains to be determined what is the best strategic response: eradication or containment.
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Kelsey, Rick G., Gladwin Joseph, and Michael G. McWilliams. "Ethanol synthesis by anoxic root segments from five cedar species relates to their habitat attributes but not their known differences in vulnerability to Phytophthora lateralis root disease." Canadian Journal of Forest Research 41, no. 6 (June 2011): 1202–11. http://dx.doi.org/10.1139/x11-043.
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Ethanol synthesis by anoxic root segments from Port Orford cedar (Chamaecyparis lawsoniana (A. Murray bis) Parl.); yellow cedar (Chamaecyparis nootkatensis (D. Don) Spach); Atlantic white cedar (Chamaecyparis thyoides (L.) Britton, Sterns & Poggenb.); western redcedar (Thuja plicata Donn ex D. Don), and incense cedar (Calocedrus decurrens (Torr.) Florin ) was compared to determine whether the amounts that they produced during flooding could contribute the known greater vulnerability of Port Orford cedar to infection by Phytophthora lateralis Tucker & Milbrat. Roots were incubated in water at 5, 15, 25, and 35 °C for 14 days with periodic sampling. After 12 h of anoxic stress, Atlantic white cedar and yellow cedar roots produced equal quantities of ethanol that were about two times more than produced by the other three species, which did not differ from one another. The roots remained anoxic for 14 days, with ethanol concentrations increasing 6 to 11 times depending on the species. After 14 days, Atlantic white cedar remained the highest ethanol producer at two to three times more than the other species, whereas incense cedar yields were the lowest. Yellow cedar, western redcedar, and Port Orford cedar had intermediate levels of ethanol. The similarity in responses of Port Orford cedar to the other species is strong evidence that ethanol is not an important contributor to its known greater vulnerability to P. lateralis infection. In general, root incubation temperature affected ethanol synthesis similarly for all species. Increases in temperature from 5 to 15 °C or 15 to 25 °C doubled the ethanol yields at 12 h. Literature ratings of anaerobic tolerance for these cedars were compared with ratings based on their ethanol yields after 12 h or 14 days of anoxia. The latter rating appears to more closely correspond with the cedars associations to wet, mesic environments and their likelihood of experiencing anoxia via flooding.
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Iqbal, Muhammad Atif, Reza Rezaee, Gregory Smith, and Partha Pratim Mandal. "Implications of thin laminations on pore structure of marine shale reservoir: Goldwyer Formation case study from Western Australia." APPEA Journal 61, no. 1 (2021): 205. http://dx.doi.org/10.1071/aj20025.
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The pore structure of a shale reservoir is a major control on hydrocarbon potential, yet shale pore systems are complex and affected by various factors. This paper focuses on the differences in pore structure between thinly laminated and massive black shale (MBSh) beds in the Ordovician Goldwyer-III shale, Canning Basin, Western Australia. A multiscale approach included image logs, core descriptions, thin sections, scanning electron microscope and X-ray diffraction analysis with low-pressure nitrogen and carbon dioxide gas adsorption tests. The results indicate that the Goldwyer shale comprises laminated beds of quartz silt and shale with thin beds of organic-rich clay, plus minor interbedded carbonate bands or concretions. The pore types are subjected to rock type, and the thinly laminated shale (LSh) is enriched in intergranular and intragranular pores. In contrast, the MBSh mainly comprises organic matter pores. The LSh is slightly enriched in mesopores but has negligible micropores. The mesopores are wedge-shaped and associated with an inorganic matrix of clay and pyrite. In comparison, the MBSh contains both mesopores and micropores. These pores are slit-like and related to organic matter and clay. The clay content and total organic carbon fluctuations control the development of mesopores and micropores in both the laminated and MBSh beds in the Goldwyer-III shale. The MBSh layers are suggested as the most important rock types for fluid flow via pore systems due to higher total pore volume, specific surface area and gas adsorption capacity.
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Zhou, Huan, Qingzhi Wang, Junmin Zhou, Tiaoying Li, Alexis Medina, Stephen Felt, Scott Rozelle, and John Openshaw. "Structural Equation Modeling (SEM) of Cysticercosis in School-Aged Children in Tibetan Rural Farming Areas of Western China: Implications for Intervention Planning." International Journal of Environmental Research and Public Health 16, no. 5 (March 4, 2019): 780. http://dx.doi.org/10.3390/ijerph16050780.
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Neurocysticercosis (NCC) significantly contributes to morbidity in developing countries. We recently published a study of prevalence and risk factors in school-aged children in three mountainous areas in Sichuan province of western China. Using structural equation modeling (SEM) on data from that study to guide intervention planning, here we examine risk factors grouped into three broad interventional categories: sociodemographics, human behavior, and sources of pork and pig husbandry. Because neuroimaging is not easily available, using SEM allows for the use of multiple observed variables (serological tests and symptoms) to represent probable NCC cases. Data collected from 2608 students was included in this analysis. Within this group, seroprevalence of cysticercosis IgG antibodies was 5.4%. SEM results showed that sociodemographic factors (β = 0.33, p < 0.05), sources of pork and pig husbandry (β = 0.26, p < 0.001), and behavioral factors (β = 0.33, p < 0.05) were all directly related to probable NCC in school-aged children. Sociodemographic factors affected probable NCC indirectly via sources of pork and pig husbandry factors (β = 0.07, p < 0.001) and behavioral variables (β = 0.07, p < 0.001). Both sociodemographic factors (β = 0.07, p < 0.05) and sources of pork and pig husbandry factors (β = 0.10, p < 0.01) affected probable NCC indirectly via behavioral variables. Because behavioral variables not only had a large direct effect but also served as a critical bridge to strengthen the effect of sociodemographics and sources of pork and pig husbandry on probable NCC, our findings suggest that interventions targeting behavioral factors may be the most effective in reducing disease.
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Zong, Yanfang, Yaqian Huang, Siyao Chen, Mingzhu Zhu, Qinghua Chen, Shasha Feng, Yan Sun, et al. "Downregulation of Endogenous Hydrogen Sulfide Pathway Is Involved in Mitochondrion-Related Endothelial Cell Apoptosis Induced by High Salt." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/754670.
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Background. The study aimed to investigate whether endogenous H2S pathway was involved in high-salt-stimulated mitochondria-related vascular endothelial cell (VEC) apoptosis.Methods. Cultured human umbilical vein endothelial cells (HUVECs) were used in the study. H2S content in the supernatant was detected. Western blot was used to detect expression of cystathionine gamma-lyase (CSE), cleaved-caspase-3, and mitochondrial and cytosolic cytochrome c (cytc). Fluorescent probes were used to quantitatively detect superoxide anion generation and measure thein situsuperoxide anion generation in HUVEC. Mitochondrial membrane pore opening, mitochondrial membrane potential, and caspase-9 activities were measured. The cell apoptosis was detected by cell death ELISA and TdT-mediated dUTP nick end labeling (TUNEL) methods.Results. High-salt treatment downregulated the endogenous VEC H2S/CSE pathway, in association with increased generation of oxygen free radicals, decreased mitochondrial membrane potential, enhanced the opening of mitochondrial membrane permeability transition pore and leakage of mitochondrial cytc, activated cytoplasmic caspase-9 and caspase-3 and subsequently induced VEC apoptosis. However, supplementation of H2S donor markedly inhibited VEC oxidative stress and mitochondria-related VEC apoptosis induced by high salt.Conclusion. H2S/CSE pathway is an important endogenous defensive system in endothelial cells antagonizing high-salt insult. The protective mechanisms for VEC damage might involve inhibiting oxidative stress and protecting mitochondrial injury.
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Li, Meng, Na Zhang, Jiao Li, Wanfeng Zhang, Wei Hei, Mengting Ji, Yang Yang, Guoqing Cao, Xiaohong Guo, and Bugao Li. "MiR-23b Promotes Porcine Preadipocyte Differentiation via SESN3 and ACSL4." Cells 11, no. 15 (July 29, 2022): 2339. http://dx.doi.org/10.3390/cells11152339.
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Genetic improvement of pork quality is one of the hot topics in pig germplasm innovation. Backfat thickness and intramuscular fat content are important indexes of meat quality. MiRNAs are becoming recognized as a crucial regulator of adipose development. Therefore, it is crucial to understand how miR-23b regulates fat metabolism at the molecular level. In the present study, Oil Red O staining, and Western blot were used to evaluate the effect of miR-23b on the differentiation of porcine preadipocytes. Dual-luciferase reporter gene assay, pulldown, and RIP were used to reveal the mechanism of miR-23b regulating cell differentiation. The findings demonstrated that miR-23b promotes the expression of adipogenic factors and increases the content of lipid droplets, thus promoting the differentiation of preadipocytes. Further research found that miR-23b can directly bind to the 3’UTR of SESN3 to regulate adipogenic differentiation. In addition, it was speculated that miR-23b controls cell differentiation by positively regulating the expression of ACSL4 in other ways. Here, we demonstrate that miR-23b promotes the differentiation of porcine preadipocytes by targeting SESN3 and promoting the expression of ACSL4. The present study is meaningful to the improvement of pork quality and the development of animal husbandry.
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Nighot, Meghali, Prashant Nighot, and Thomas Ma. "PROTON PUMP INHIBITORS (PPI) INDUCES COLONIC TIGHT JUNCTION BARRIER (TJ) DYSFUNCTION VIA AN UPREGULATION OF TJ PORE FORMING CALUDIN-2 PROTEIN." Inflammatory Bowel Diseases 27, Supplement_1 (January 1, 2021): S27—S28. http://dx.doi.org/10.1093/ibd/izaa347.062.
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Abstract Background Proton pump inhibitors (PPIs) are highly effective antagonists of gastric acid secretion and are widely used to treat a number of gastroesophageal disorders, including peptic ulcer disease, GERD, and Barrett’s esophagus. PPI-induced elevation in intra-gastric pH and subsequent alterations of gastrointestinal physiology are thought to cause undesired effects on the entire GI tract. Defective intestinal Tight Junction (TJ) barrier is an important pathogenic factor for intestinal inflammation. Claudin-2 is a pore forming TJ protein whose overexpression causes selective increase in TJ permeability to small molecules. Claudin-2 expression is known to be up-regulated in intestinal inflammation and inflammation-associated colon carcinogenesis. The effect of PPI on Intestinal TJ barrier is not known. Aim: The aim of the present study was to study the effect of PPI on Intestinal TJ permeability. Methods A cell culture model of filter grown human intestinal epithelial Caco-2 monolayers, was used to study intestinal epithelial TJ barrier function. The mouse colonic permeability was measured by Ussing chambers studies. Western blot (WB) and Immunofluorescence (IF) was used to study the protein expression of claudin-2 in Caco-2 cells and in mouse colon. Cell surface biotinylation was used to study intracellular trafficking of TJ proteins. Results PPIs, caused a concentration- and time-dependent decrease in transepithelial resistance (TER), and increase in urea flux in filter-grown Caco-2 cells. Further studies on intestinal TJ revealed that PPI caused a significant increase in pore forming TJ protein claudin-2 protein level (western blot), but not mRNA (RT-PCR) in Caco-2 monolayers. Claudin-2 was co-localized to its known intercellular trafficking vesicles, clathrin pits. PPI treatment caused an increase in expression and junctional localization of claudin-2 and a decrease in its cytoplasmic co-localization with clathrin. Similarly, pulse-chase assay showed that the claudin-2 half-life was increased by PPI. In cell surface biotinylation assay, the rate of claudin-2 endocytosis was significantly reduced by PPI. In ex-vivo, Ussing chamber studies, PPI administration for 45 days resulted in a significant decrease in murine colonic TER and increase in urea flux. Immunofluorescence and Western blot analysis showed that PPI also caused an increase in TJ protein claudin-2 expression in mice colonic mucosa. Conclusion Our results suggest that the PPIs induces colonic TJ permeability via increasing pore forming claudin-2 levels. PPIs affect intracellular trafficking to reduce claudin-2 degradation and increased its junctional localization.
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Pravdic, Danijel, Filip Sedlic, Yasushi Mio, Nikolina Vladic, Martin Bienengraeber, and Zeljko J. Bosnjak. "Anesthetic-induced Preconditioning Delays Opening of Mitochondrial Permeability Transition Pore via Protein Kinase C-ϵ–mediated Pathway." Anesthesiology 111, no. 2 (August 1, 2009): 267–74. http://dx.doi.org/10.1097/aln.0b013e3181a91957.
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Background Cardioprotection by volatile anesthetic-induced preconditioning (APC) involves activation of protein kinase C (PKC). This study investigated the importance of APC-activated PKC in delaying mitochondrial permeability transition pore (mPTP) opening. Methods Rat ventricular myocytes were exposed to isoflurane in the presence or absence of nonselective PKC inhibitor chelerythrine or isoform-specific inhibitors of PKC-delta (rottlerin) and PKC-epsilon (myristoylated PKC-epsilon V1-2 peptide), and the mPTP opening time was measured by using confocal microscopy. Ca-induced mPTP opening was measured in mitochondria isolated from rats exposed to isoflurane in the presence and absence of chelerythrine or in mitochondria directly treated with isoflurane after isolation. Translocation of PKC-epsilon was assessed in APC and control cardiomyocytes by Western blotting. Results In cardiomyocytes, APC prolonged time necessary to induce mPTP opening (261 +/- 26 s APC vs. 216 +/- 27 s control; P < 0.05), and chelerythrine abolished this delay to 213 +/- 22 s. The effect of isoflurane was also abolished when PKC-epsilon inhibitor was applied (210 +/- 22 s) but not in the presence of PKC-delta inhibitor (269 +/- 31 s). Western blotting revealed translocation of PKC-epsilon toward mitochondria in APC cells. The Ca concentration required for mPTP opening was significantly higher in mitochondria from APC rats (45 +/- 8 microM x mg control vs. 64 +/- 8 microM x mg APC), and APC effect was reversed with chelerythrine. In contrast, isoflurane did not protect directly treated mitochondria. Conclusion APC induces delay of mPTP opening through PKC-epsilon mediated inhibition of mPTP opening, but not through PKC-delta. These results point to the connection between cytosolic and mitochondrial components of cardioprotection by isoflurane.
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Linden, Jennifer, Kiel Telesford, Samantha Shetty, Paige Winokour, Sylvia Haigh, Ellen Cahir-McFarland, Giovanna Antognetti, et al. "A Novel Panel of Rabbit Monoclonal Antibodies and Their Diverse Applications Including Inhibition of Clostridium perfringens Epsilon Toxin Oligomerization." Antibodies 7, no. 4 (October 25, 2018): 37. http://dx.doi.org/10.3390/antib7040037.
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The pore-forming epsilon toxin (ETX) produced by Clostridium perfringens is among the most lethal bacterial toxins known. Sensitive antibody-based reagents are needed to detect toxin, distinguish mechanisms of cell death, and prevent ETX toxicity. Using B-cell immuno-panning and cloning techniques, seven ETX-specific monoclonal antibodies were generated from immunized rabbits. ETX specificity and sensitivity were evaluated via western blot, ELISA, immunocytochemistry (ICC), and flow cytometry. ETX-neutralizing function was evaluated both in vitro and in vivo. All antibodies recognized both purified ETX and epsilon protoxin via western blot with two capable of detecting the ETX-oligomer complex. Four antibodies detected ETX via ELISA and three detected ETX bound to cells via ICC or flow cytometry. Several antibodies prevented ETX-induced cell death by either preventing ETX binding or by blocking ETX oligomerization. Antibodies that blocked ETX oligomerization inhibited ETX endocytosis and cellular vacuolation. Importantly, one of the oligomerization-blocking antibodies was able to protect against ETX-induced death post-ETX exposure in vitro and in vivo. Here we describe the production of a panel of rabbit monoclonal anti-ETX antibodies and their use in various biological assays. Antibodies possessing differential specificity to ETX in particular conformations will aid in the mechanistic studies of ETX cytotoxicity, while those with ETX-neutralizing function may be useful in preventing ETX-mediated mortality.
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Sammaljärvi, Juuso, Antero Lindberg, Jussi Ikonen, Mikko Voutilainen, Marja Siitari-Kauppi, and Lasse Koskinen. "Investigation of mineralogy, porosity and pore structure of Olkiluoto bedrock." MRS Proceedings 1665 (2014): 31–37. http://dx.doi.org/10.1557/opl.2014.625.
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ABSTRACTSpent nuclear fuel from TVO's (Teollisuuden Voima Oy) and Fortum's nuclear power plants will be deposited deep in the crystalline bedrock in Olkiluoto, Western Finland. The bedrock needs to be well characterized to assess the risks inherent to the waste disposal at the site. If radionuclides (RN) are transported, it happens via water conducting fractures. Retardation may occur either by diffusion into stagnant pore water or by immobilization on mineral surfaces of the rock matrix.RN’s retardation from flowing water is linked to parameters defining porosity and microscopic rock pore structure, such as pore size distribution, connectivity, tortuosity and constrictivity, and by the mineralogy and chemical nature of the minerals and charge of the pore surfaces.In this work, centimeter scale rock cores from Olkiluoto were investigated. The work is part of the in situ project REPRO (Experiments to investigate Rock Matrix Retention Properties) where the diffusion and sorption of RN are studied experimentally. Porosity and pore structures were characterized with the PMMA autoradiography method and polarized microscopy, which was used also to ascertain the mineralogy of the samples.The results show that the rock from the REPRO site has low porosity with a mean value of 0.5% and a range of 0.1-1.5%. Rock heterogeneity explains the variation of porosity values. Correlation between the porosity and the mineralogy was found. Areas of high porosity correspond to areas of altered minerals, such as cordierite, biotite and plagioclase, which cover spatially between 10 and 20% of the rock volume
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Bryan, Robert M., Junping You, Sharon C. Phillips, Jon J. Andresen, Eric E. Lloyd, Paul A. Rogers, Stuart E. Dryer, and Sean P. Marrelli. "Evidence for two-pore domain potassium channels in rat cerebral arteries." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 2 (August 2006): H770—H780. http://dx.doi.org/10.1152/ajpheart.01377.2005.
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Little is known about the presence and function of two-pore domain K+ (K2P) channels in vascular smooth muscle cells (VSMCs). Five members of the K2P channel family are known to be directly activated by arachidonic acid (AA). The purpose of this study was to determine 1) whether AA-sensitive K2P channels are expressed in cerebral VSMCs and 2) whether AA dilates the rat middle cerebral artery (MCA) by increasing K+ currents in VSMCs via an atypical K+ channel. RT-PCR revealed message for the following AA-sensitive K2P channels in rat MCA: tandem of P domains in weak inward rectifier K+ (TWIK-2), TWIK-related K+ (TREK-1 and TREK-2), TWIK-related AA-stimulated K+ (TRAAK), and TWIK-related halothane-inhibited K+ (THIK-1) channels. However, in isolated VSMCs, only message for TWIK-2 was found. Western blotting showed that TWIK-2 is present in MCA, and immunohistochemistry further demonstrated its presence in VSMCs. AA (10–100 μM) dilated MCAs through an endothelium-independent mechanism. AA-induced dilation was not affected by inhibition of cyclooxygenase, epoxygenase, or lipoxygenase or inhibition of classical K+ channels with 10 mM TEA, 3 mM 4-aminopyridine, 10 μM glibenclamide, or 100 μM Ba2+. AA-induced dilations were blocked by 50 mM K+, indicating involvement of a K+ channel. AA (10 μM) increased whole cell K+ currents in dispersed cerebral VSMCs. AA-induced currents were not affected by inhibitors of the AA metabolic pathways or blockade of classical K+ channels. We conclude that AA dilates the rat MCA and increases K+ currents in VSMCs via an atypical K+ channel that is likely a member of the K2P channel family.
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Dean, Tim. "Genre Blindness in the New Descriptivism." Modern Language Quarterly 81, no. 4 (December 1, 2020): 527–52. http://dx.doi.org/10.1215/00267929-8637950.
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Abstract This essay considers the “descriptive turn” in literary studies from the vantage point of poetics, arguing that the history of Western poetry, from the Greeks to the present, offers through the category of epideixis a theory and practice of description that illuminates some of the methodological impasses of contemporary literary studies. Epideixis, a basic mode of pointing or linguistic ostension, confers value, often by way of praise or blame, without trying to persuade its audience with the practical immediacy of political or forensic rhetoric. Drawing on the ordinary language philosophy of Ludwig Wittgenstein and Stanley Cavell, the essay suggests that praise constitutes a philosophically rigorous alternative to critique. This argument is exemplified via the work of Mark Doty, a contemporary poet of description-as-praise.
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Pendoley, K. L., P. A. Whittock, A. Vitenbergs, and C. Bell. "Twenty years of turtle tracks: marine turtle nesting activity at remote locations in the Pilbara, Western Australia." Australian Journal of Zoology 64, no. 3 (2016): 217. http://dx.doi.org/10.1071/zo16021.
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Little is known about the biology and ecology of marine turtles in the Pilbara region of Western Australia and most potential habitat is unconfirmed and, therefore, undescribed. Understanding basic biological parameters at a regional level is critically important for effective long-term management. We used the ‘track census’ methodology to identify reproductive habitat and assess species-specific abundance of adult flatback (Natator depressus), green (Chelonia mydas) and hawksbill (Eretmochelys imbricata) turtles at 154 locations in the Pilbara region of Western Australia. Between 1992 and 2012, potential nesting habitat was assessed via either ground or aerial ‘snapshot’ (single visit) or ‘census’ (more than one night) surveys and additional information obtained using the Expert Elicitation Method. Species-specific abundance (tracks night–1 ± s.d.) was varied; green turtles were most abundant, nesting at fewer locations (n = 47) but in greater numbers (1200.5 ± 62.0) than flatback or hawksbill turtles and primarily (93%) at island locations. Flatback turtle nests were more widely distributed (n = 77) than those of green or hawksbill turtles, yet abundance (877.4 ± 29.5) was lower than that of green and greater than that of hawksbill turtles. Activity was primarily (76%) island-based and activity on the mainland coastline was concentrated close to Mundabullangana and Cemetery Beach. Hawksbill turtle abundance (314.1 ± 17.1) was lowest and the least widespread (n = 43), concentrated primarily in the Onslow and Dampier subregions with no activity recorded in the Port Hedland subregion or on the mainland coastline. The findings provide information with which the Federal government can meaningfully assess the status and distribution of EPBC Act–listed species where habitat overlaps with areas zoned for development. We highlight the urgent need for the Federal Government to regulate the process by which we accumulate data to support data quality and provide meaningful information to enhance efficacy in state and Federal management of species of concern.
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Zhang, Yunfang, Junxia Feng, Qi Wang, Shili Zhao, Shen Yang, Lu Tian, Ping Meng, Jingchun Li, and Hongyan Li. "Hyperglycaemia Stress-Induced Renal Injury is Caused by Extensive Mitochondrial Fragmentation, Attenuated MKP1 Signalling, and Activated JNK-CaMKII-Fis1 Biological Axis." Cellular Physiology and Biochemistry 51, no. 4 (2018): 1778–98. http://dx.doi.org/10.1159/000495681.
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Background/Aims: Hyperglycaemia stress-induced renal injury is closely associated with mitochondrial dysfunction through poorly understood mechanisms. The aim of our study is to explore the upstream trigger and the downstream effector driving diabetic nephropathy via modulating mitochondrial homeostasis. Methods: A diabetic nephropathy model was generated in wild-type (WT) mice and MAP Kinase phosphatase 1 transgenic (MKP1-TG) mice using STZ injection. Cell experiments were conducted via high-glucose treatment in the human renal mesangial cell line (HRMC). MKP1 overexpression assay was carried out via adenovirus transfection. Renal function was evaluated via ELISA, western blotting, histopathological staining, and immunofluorescence. Mitochondrial function was determined via mitochondrial potential analysis, ROS detection, ATP measurement, mitochondrial permeability transition pore (mPTP) opening evaluation, and immunofluorescence for mitochondrial pro-apoptotic factors. Loss- and gain-of-function assays for mitochondrial fragmentation were performed using a pharmacological agonist and blocker. Western blotting and the pathway blocker were used to establish the signalling pathway in response to MKP1 overexpression in the presence of hyperglycaemia stress. Results: MKP1 was downregulated in the presence of chronic high-glucose stress in vivo and in vitro. However, MKP1 overexpression improved the metabolic parameters, enhanced glucose control, sustained renal function, attenuated kidney oxidative stress, inhibited the renal inflammation response, alleviated HRMC apoptosis, and repressed tubulointerstitial fibrosis. Molecular investigation found that MKP1 overexpression enhanced the resistance of HRMC to the hyperglycaemic injury by abolishing mitochondrial fragmentation. Hyperglycaemia-triggered mitochondrial fragmentation promoted mitochondrial dysfunction, as evidenced by decreased mitochondrial potential, elevated mitochondrial ROS production, increased pro-apoptotic factor leakage, augmented mPTP opening and activated caspase-9 apoptotic pathway. Interestingly, MKP1 overexpression strongly abrogated mitochondrial fragmentation and sustained mitochondrial homeostasis via inhibiting the JNK-CaMKII-Fis1 pathway. After re-activation of the JNK-CaMKII-Fis1 pathway, the beneficial effects of MKP1 overexpression on mitochondrial protection disappeared. Conclusion: Taken together, our data identified the protective role played by MKP1 in regulating diabetic renal injury via repressing mitochondrial fragmentation and inactivating the JNK-CaMKII-Fis1 pathway, which may pave the road to new therapeutic modalities for the treatment of diabetic nephropathy.
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Wang, Liqin, Ying-Hong Feng, and George I. Gorodeski. "Epidermal Growth Factor Facilitates Epinephrine Inhibition of P2X7-Receptor-Mediated Pore Formation and Apoptosis: A Novel Signaling Network." Endocrinology 146, no. 1 (January 1, 2005): 164–74. http://dx.doi.org/10.1210/en.2004-1026.
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Epidermal growth factor (EGF), epinephrine, and the P2X7 receptor system regulate growth of human uterine cervical epithelial cells, but little is known about how these systems intercommunicate in exerting their actions. The objective of this study was to understand the mechanisms of EGF and epinephrine regulation of growth of cervical cells. Treatment of cultured CaSki cells with 0.2 nm EGF increased cell number via a PD98059-sensitive pathway. Treatment with 2 nm epinephrine increased cell number, and the effect was facilitated by cotreatment with EGF. Whereas the effect of EGF alone involved up-regulation of [3H]-thymidine incorporation and an increase in cell proliferation, the effect of epinephrine was mediated by inhibition of apoptosis. Epinephrine inhibited apoptosis induced by the P2X7 receptor ligand 2′,3′-0-(4-benzoylbenzoyl)-ATP, by attenuation of P2X7 receptor plasma membrane pore formation. Cotreatment with EGF facilitated epinephrine effect via a phosphoinositide 3-kinase-dependent mechanism. CaSki cells express the β2-adrenoceptor, and the epinephrine antiapoptotic effect could be mimicked by β2-adrenoceptor agonists and by activators of adenylyl cyclase. Likewise, the effect could be blocked by β2-adrenoceptor blockers and by the inhibitor of protein kinase-A H-89. Western immunoblot analysis revealed that epinephrine decreased the levels of the glycosylated 85-kDa form of the P2X7 receptor and increased receptor degradation, and that EGF potentiated these effects of epinephrine. EGF did not affect cellular levels of the β2-adrenoceptor. In contrast, EGF, acting via the EGF receptor, augmented β2-adrenoceptor recycling, and it inhibited β2-adrenoceptor internalization via a phosphoinositide 3-kinase-dependent mechanism. We conclude that, in cervical epithelial cells, EGF has a dual role: as mitogen, acting via the MAPK/MAPK kinase pathway, and as an antiapoptotic factor by facilitating epinephrine effect and resulting in greater expression of β2-adrenoceptors in the plasma membrane. These findings underscore a novel signaling network of communication between the receptor tyrosine kinases, the G protein-coupled receptors, and the purinergic P2X7 receptor.
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Ito, Satoshi, Jaime Bosch, Cristina Jurado, José Manuel Sánchez-Vizcaíno, and Norikazu Isoda. "Risk Assessment of African Swine Fever Virus Exposure to Sus scrofa in Japan Via Pork Products Brought in Air Passengers’ Luggage." Pathogens 9, no. 4 (April 20, 2020): 302. http://dx.doi.org/10.3390/pathogens9040302.
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In recent years, African swine fever (ASF) has become prevalent in many areas, including Asia. The repeated detection of the ASF virus (ASFV) genome in pork products brought in air passenger’s luggage (PPAP) was also reported from Japanese airports. In the present study, the risk of ASFV exposure to susceptible hosts in Japan via three different pathways was assessed. Two quantitative stochastic risk assessment models were built to estimate the annual probability of ASFV exposure to domestic pigs, which could be attributed to foreign job trainees or foreign tourists. A semi-quantitative stochastic model was built to assess the risk of ASFV exposure to wild boar caused by foreign tourists. The overall mean annual probability of ASFV exposure to domestic pigs via PPAP carried by foreign job trainees was 0.169 [95% confidence interval (CI): 0.000–0.600], whereas that by foreign tourists was 0.050 [95% CI: 0.000–0.214], corresponding to approximately one introduction every 5.9 and 20 years, respectively. The risk of ASFV exposure to domestic pigs was dispersed over the country, whereas that of wild boar was generally higher in the western part of Japan, indicating that the characteristics of the potential ASF risk in each prefecture were varied.
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Manevy, Federico, Gabriele Filkauskas, Pierre Levy, Judy Fredriksson, and Jesse Sussell. "Potential non-drug cost differences associated with the use of the fixed-dose combination of pertuzumab and trastuzumab for subcutaneous injection (PH FDC SC) in the treatment of HER2-positive early breast cancer patients in Western Europe and the United States." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): 544. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.544.
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544 Background: In patients with HER2-positive early breast cancer (BC), pertuzumab (P) added to trastuzumab (T) and chemotherapy has been recognized as a standard-of-care, improving the risk of recurrence. P and T treatments can be given intravenously (PT IV) or, more recently, subcutaneously − via PH FDC SC. Both methods are comparable in terms of efficacy and safety profiles. However, PH FDC SC allows for a faster infusion than that of PT IV, and this can be associated with lower costs. The aim of this study is to estimate the incremental difference in non-drug costs between PH FDC SC and PT IV for a typical patient receiving treatment for HER2-positive early BC in Western Europe and the United States. Methods: A model-based cost-minimization analysis was performed to quantify mean non-drug cost differences per patient over a full course of therapy (18 cycles). Western Europe: costs in the analysis are based on an archetypal country, and explicitly include estimates for costs for patient chair time, active healthcare professional (HCP) time, usage of non-drug consumables, port-a-cath placement surgeries and patients’ productivity losses. Costs are calculated by multiplying the resource use by its corresponding unit price. Costing data were obtained from literature sources on T SC time and cost savings for Western European countries, and assumptions on PH FDC SC and PT IV times and costs. United States: non-drug costs for the two strategies were estimated using average net reimbursement amounts for relevant procedure codes for intravenous and SC therapy administration among commercial payers in the MarketScan databases. Results: PH FDC SC is estimated to reduce non-drug costs by 73% − 80% in Western Europe, and 75% in the United States. Total monetary non-drug savings per patient over 18 cycles of treatment are estimated in the range of €2,474 − €8,975 in Western Europe, and at $10,138 in the United States. In Western Europe, where the analysis allows for a disaggregation by cost category, cost savings related to savings in patient chair time (excluding patients’ productivity losses) are estimated to account for up to 62% of overall non-drug cost savings. Patients’ productivity losses are estimated to explain up to 11% of non-drug cost differences. Conclusions: The use of PH FDC SC for the treatment of HER2-positive BC can potentially result in substantial non-drug cost savings. These savings could easily derive in overall net cost savings to the healthcare system, contributing to the long-term sustainability of the healthcare spending, while still providing a safe and effective therapy.[Table: see text]
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Lemoine, Sandrine, Lan Zhu, Damien Legallois, Massimo Massetti, Alain Manrique, and Jean-Luc Hanouz. "Atorvastatin-induced Cardioprotection of Human Myocardium Is Mediated by the Inhibition of Mitochondrial Permeability Transition Pore Opening via Tumor Necrosis Factor-α and Janus Kinase/Signal Transducers and Activators of Transcription Pathway." Anesthesiology 118, no. 6 (June 1, 2013): 1373–84. http://dx.doi.org/10.1097/aln.0b013e31828a7039.
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Abstract Background: The role of tumor necrosis factor-α (TNF-α), Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, and mitochondrial Permeability Transition Pore in atorvastatin-induced cardioprotection were examined in human myocardium, in vitro. Methods: Isometric force of contraction of human right atrial trabeculae was recorded during 30-min hypoxia and 60-min reoxygenation (control) and in the presence of atorvastatin (0.1 µm, 1 µm, 10 µm). In early reoxygenation, the TNF-α inhibitor, AG490 (inhibitor of JAK/STAT), or atractyloside (mitochondrial Permeability Transition Pore opener), were administered. Cyclosporine A (inhibitor of mitochondrial Permeability Transition Pore opening) was administered during the first minute of reoxygenation alone or in presence of atorvastatin and TNF-α inhibitor or AG490. The force of contraction (percentage of baseline) at the end of reoxygenation period was compared (mean ± SD; n = 6 in each group). Protein expression of JAK/STAT pathway was measured using Western immunoblotting. Results: Atorvastatin 0.1 µm (70 ± 9%), 1 µm (85 ± 5%), 10 µm (89 ± 5%), and Cyclosporine A (87 ± 10%) improved the recovery of force of contraction at the end of reoxygenation, as compared with control (50 ± 3%). Atorvastatin 1 µm (4.64 ± 2.90ng · ml−1 · g−1 of tissue) decreased the release of troponin Ic after hypoxia-reoxygenation (control: 26.34 ± 19.30ng · ml−1 · g−1; P < 0.001). The enhanced recovery of force of contraction after atorvastatin administration was abolished by TNF-α inhibitor (53 ± 8%), AG490 (56 ± 7%), atractyloside (48 ± 8%). Cyclosporine A restored the atorvastatin-induced cardioprotection abolished by TNF-α inhibitor (87 ± 6%) and AG490 (83 ± 9%). Atorvastatin significantly increased the phosphorylation of JAK-2 and STAT-3, TNF-α inhibitor abolished the enhanced phosphorylation of JAK-2 and STAT-3 by atorvastatin. Conclusions: Atorvastatin-induced cardioprotection involved the inhibition of the mitochondrial Permeability Transition Pore opening via the activation of TNF-α and the JAK/STAT pathway in early reoxygenation.
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Chen, Songfeng, Qing Tian, Chunfeng Shang, Lin Yang, Na Wei, Guowei Shang, Yanhui Ji, Hongwei Kou, Shitao Lu, and Hongjian Liu. "Synergistic Utilization of Necrostatin-1 and Z-VAD-FMK Efficiently Promotes the Survival of Compression-Induced Nucleus Pulposus Cells via Alleviating Mitochondrial Dysfunction." BioMed Research International 2020 (December 8, 2020): 1–12. http://dx.doi.org/10.1155/2020/6976317.
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We recently reported that necroptosis contributed to compression-induced nucleus pulposus (NP) cells death. In the current study, we investigated the regulative effect of necroptosis inhibitor Necrostatin-1 on NP cells apoptosis and autophagy. Necrostatin-1, autophagy inhibitor 3-Methyladenine and apoptosis inhibitor Z-VAD-FMK were employed, and NP cells were exposed to 1.0 MPa compression for 0, 24 and 36 h. Necroptosis-associated molecules were measured by Western blot and RT-PCR. Autophagy and apoptosis levels were evaluated by Western blot and quantified by flow cytometry after monodansylcadaverine and Annexin V-FITC/propidium iodide staining, respectively. The cell viability and cell death were also examined. Furthermore, we measured mitochondrial membrane potential (MMP), mitochondrial permeability transition pore (MPTP) and indices of oxidative stress to assess mitochondrial dysfunction. The results established that Necrostatin-1 blocked NP cells autophagy, and 3-Methyladenine had little influence on NP cells necroptosis. The Necrostatin-1+3-Methyladenine treatment exerted almost the same role as Necrostatin-1 in reducing NP cells death. Necrostatin-1 restrained NP cells apoptosis, while Z-VAD-FMK enhanced NP cells necroptosis. The Necrostatin-1+Z-VAD-FMK treatment provided more prominent role in blocking NP cells death compared with Necrostatin-1, consistent with increased MMP, reduced opening of MPTP and oxidative stress. In summary, the synergistic utilization of Necrostatin-1 and Z-VAD-FMK is a very worthwhile solution in preventing compression-mediated NP cells death, which might be largely attributed to restored mitochondrial function.
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Agius, Dionisius A. "The Rashayda: Ethnic Identity and Dhow Activity in Suakin on the Red Sea Coast." Northeast African Studies 12, no. 1 (April 1, 2012): 169–216. http://dx.doi.org/10.2307/41960562.
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Abstract Suakin (Ar. Sawākin) is the second important town of Sudan and a port for Muslim pilgrims bound for Jeddah Its economy is primarily based on fishing. Long before the estabhshment of the present, new town, Suakin was an island town to which cargo ships from the Red Sea ports came and goods from India were transhipped via Jeddah In its heyday, the island town was populated by merchants and traders who came to settle there from African and Arab countnes, mainly Egypt and Sudan, and India and Europe. The majonty of the inhabitants who lived around the island town belonged to the Beja (Ar. Buja or Bujā) groupings, whose ancestry goes back centwies; they were, as they are mainly today, pastorahsts and cultivators. Around the late nineteenth century, members of a distinct Western Arabian ethnic group, the Rashayda (Ar. Rashāʾida; s. Rashīdī), came to Sudan to look for work and live in the hinterland and on the coast. Though the majonty were nomads and herders, several were involved in dhow trading, and a small number settled in Suakin. By the 1930s, however, many buildings in the island town started to crumble into rubble as its inhabitants abandoned the island for better economic prospects in other Red Sea port towns. Subsequently, a new town developed south of the island, including communities from the neighboring region, mainly Cushitic-speaking Beja groupings and other minorities such as the Rashayda, and in recent decades, they were joined by West African pilgrims who chose to settle there on their return from hajj (pilgrimage). Some members of the Beja groups follow occupations related to the sea; many come from the mountains to seek work as fishermen, or divers during the shell-collecting season, or laborers during the hajj season. Fishing activity is centered on the craftsmanship of the dhow builders: the dhows must not only be seaworthy but also specifically designed for fishing and shell collecting. This article will examine maritime activity on the Sudanese coast with particular reference to Suakin, past and present. It will discuss the level of involvement of the Beja and the importance of the role of the Rashayda in this multiethnic community from their arrival in the nineteenth century to the present time; further, it will show how they adapted their knowledge and skills and also show that the maritime terminology used is predominantly Western Arabian and not, as would be expected, Cushitic, as spoken by the Beja groups or linguistic registers of other ethnic groupings. The methodology applied in this research is based on ethnographic fieldwork conducted in 2004, together with consultation of primary and secondary sources.
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Carvalho, Rafael C., and Ruth Reef. "Quantification of Coastal Change and Preliminary Sediment Budget Calculation Using SfM Photogrammetry and Archival Aerial Imagery." Geosciences 12, no. 10 (September 26, 2022): 357. http://dx.doi.org/10.3390/geosciences12100357.
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A preliminary sediment budget for the sandy shores flanking the entrance to Western Port, a large bay in Australia, was formulated using a comparison between two Digital Surface Models (DSMs) with a 30-year interval and auxiliary shoreline data. The 1977 DSM was generated from ten aerial photographs using Structure-from-Motion (SfM) photogrammetry. Assessment of its accuracy obtained an RMSE of 0.48 m with most of the independent points overpredicting or underpredicting elevations by less than 0.5 m following manual point cloud cleaning. This technique created a 7.5 km2 surface with a Ground Sampling Distance of 34.3 cm between two coastal towns separated by a narrow channel. Comparison of the 1977 DSM to a second, light detection and ranging (LiDAR)-derived DSM from 2007 showed that a volume of ~200,000 m3 of sediment (above Mean Sea Level) was deposited at Newhaven Beach on Phillip Island, while, during the same period, ~40,000 m3 of sediment was lost from the mainland beaches of San Remo, on the eastern side of the channel. Shoreline positions extracted from aerial photographs taken in 1960 and a nautical chart published one century earlier indicate that the progradation experienced at Newhaven Beach has been possible due to provision of sediment via destabilisation of the vegetation covering the updrift Woolamai isthmus on the southeast coast of Phillip Island, whereas the retreat observed at San Remo Beach since 1960 can be attributed to the natural dynamics of the entrance, which appears to favour flood-dominance on the western side and ebb-dominance on the eastern side. While a more comprehensive balance of volumes entering and exiting the area would specifically benefit from volumetric assessments of the subaqueous part of the entrance, the general usefulness of quantifying coastal change using SfM and historical photographs is demonstrated.
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Yao, Chaogang, Daxin Pang, Chao Lu, Aishi Xu, Peixuan Huang, Hongsheng Ouyang, and Hao Yu. "Data Mining and Validation of AMPK Pathway as a Novel Candidate Role Affecting Intramuscular Fat Content in Pigs." Animals 9, no. 4 (April 1, 2019): 137. http://dx.doi.org/10.3390/ani9040137.
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Intramuscular fat (IMF) is an important economic trait for pork quality and a complex quantitative trait regulated by multiple genes. The objective of this work was to investigate the novel transcriptional effects of a multigene pathway on IMF deposition in the longissimus dorsi (LD) muscles of pigs. Potential signaling pathways were screened by mining data from three gene expression profiles in the Gene Expression Omnibus (GEO) database. We designed quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) arrays for the candidate signaling pathways to verify the results in the LD muscles of two pig breeds with different IMF contents (Large White and Min). Western blot analysis was used to detect the expression levels of several candidate proteins. Our results showed that the AMPK signaling pathway was screened via bioinformatics analysis. Ten key hub genes of this signaling pathway (AMPK, ADIPOR1, ADIPOR2, LKB1, CAMKKβ, CPT1A, CPT1B, PGC-1α, CD36, and ACC1) were differentially expressed between the Large White and Min pigs. Western blot analysis further confirmed that LKB1/CaMKK2-AMPK-ACC1-CPT1A axis dominates the activity of AMPK signaling pathway. Statistical analyses revealed that AMPK signaling pathway activity clearly varied among the two pig breeds. Based on these results, we concluded that the activation of the AMPK signaling pathway plays a positive role in reducing IMF deposition in pigs.
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Price, Katherine E., and Andrew Camilli. "Pneumolysin Localizes to the Cell Wall of Streptococcus pneumoniae." Journal of Bacteriology 191, no. 7 (January 23, 2009): 2163–68. http://dx.doi.org/10.1128/jb.01489-08.
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ABSTRACT Streptococcus pneumoniae is the causative agent of multiple diseases, including otitis media, pneumonia, bacteremia, and meningitis. Pneumolysin (Ply), a member of the cholesterol-dependent cytolytic pore-forming toxins, is produced by virtually all clinical isolates of S. pneumoniae, and strains in which the Ply gene has been deleted are severely attenuated in mouse models of infection. In contrast to all other members of the cholesterol-dependent cytolysin family, Ply lacks a signal peptide for export. Instead, Ply has been hypothesized to be released upon autolysis or, alternatively, via a nonautolytic mechanism that remains ill defined. We determined by use of cell fractionation and Western blotting that, during in vitro growth, exported Ply is localized primarily to the cell wall compartment in 18 different serotypes in the absence of detectable cell lysis. Hemolytic assays revealed that this cell wall-localized Ply is active. Additionally, cell wall-localized Ply is accessible to extracellular protease and is detergent releasable.
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Zeng, Hong, Yadong Wang, Haoying Han, Yanping Cao, and Bei Wang. "Changes in Key Aroma Compounds and Esterase Activity of Monascus-Fermented Cheese across a 30-Day Ripening Period." Foods 11, no. 24 (December 13, 2022): 4026. http://dx.doi.org/10.3390/foods11244026.
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Monascus-fermented cheese (MC) is a new type of mold-ripened cheese that combines a traditional Chinese fermentation fungus, Monascus purpureus M1, with Western cheese fermentation techniques. In this study, the compositions of the volatile aroma compounds in MC were analyzed during a 30-day ripening period using SPME-Arrow and GC-O-MS. The activity of esterase in MC, which is a key enzyme catalyzing esterification reaction, was determined and compared with the control group (CC). Next, sensory analysis was conducted via quantitative descriptive analysis followed by Pearson correlation analysis between esterase activity and the key flavor compounds. A total of 76 compounds were detected. Thirty-three of these compounds could be smelled at the sniffing port and were identified as the key aroma compounds. The esterase activity in MC was found to be 1.24~1.33 times that of the CC. Moreover, the key odor features of ripened MC were alcohol and fruity flavors, considerably deviating from the sour and cheesy features found for the ripened CC. Furthermore, correlation analysis showed that esterase activity was strongly correlated (|r|> 0.75, p < 0.05) with various acids such as pentanoic and nonanoic acids and several aromatic esters, namely, octanoic acid ethyl ester and decanoic acid ethyl ester, revealing the key role that esterases play in developing the typical aroma of ripened MC.
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Qiao, Shigang, Jessica M. Olson, Mark Paterson, Yasheng Yan, Ivan Zaja, Yanan Liu, Matthias L. Riess, et al. "MicroRNA-21 Mediates Isoflurane-induced Cardioprotection against Ischemia–Reperfusion Injury via Akt/Nitric Oxide Synthase/Mitochondrial Permeability Transition Pore Pathway." Anesthesiology 123, no. 4 (October 1, 2015): 786–98. http://dx.doi.org/10.1097/aln.0000000000000807.
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Abstract Background: The role of microRNA-21 in isoflurane-induced cardioprotection is unknown. The authors addressed this issue by using microRNA-21 knockout mice and explored the underlying mechanisms. Methods: C57BL/6 and microRNA-21 knockout mice were echocardiographically examined. Mouse hearts underwent 30 min of ischemia followed by 2 h of reperfusion in vivo or ex vivo in the presence or absence of 1.0 minimum alveolar concentration of isoflurane administered before ischemia. Cardiac Akt, endothelial nitric oxide synthase (eNOS), and neuronal nitric oxide synthase (nNOS) proteins were determined by Western blot analysis. Opening of the mitochondrial permeability transition pore (mPTP) in cardiomyocytes was induced by photoexcitation-generated oxidative stress and detected by rapid dissipation of tetramethylrhodamine ethyl ester fluorescence using a confocal microscope. Results: Genetic disruption of miR-21 gene did not alter phenotype of the left ventricle, baseline cardiac function, area at risk, and the ratios of phosphorylated-Akt/Akt, phosphorylated-eNOS/eNOS, and phosphorylated-nNOS/nNOS. Isoflurane decreased infarct size from 54 ± 10% in control to 36 ± 10% (P < 0.05, n = 8 mice per group), improved cardiac function after reperfusion, and increased the ratios of phosphorylated-Akt/AKT, phosphorylated-eNOS/eNOS, and phosphorylated-nNOS/nNOS in C57BL/6 mice subjected to ischemia–reperfusion injury. These beneficial effects of isoflurane were lost in microRNA-21 knockout mice. There were no significant differences in time of the mPTP opening induced by photoexcitation-generated oxidative stress in cardiomyocytes isolated between C57BL/6 and microRNA-21 knockout mice. Isoflurane significantly delayed mPTP opening in cardiomyocytes from C57BL/6 but not from microRNA-21 knockout mice. Conclusions: Isoflurane protects mouse hearts from ischemia–reperfusion injury by a microRNA-21-dependent mechanism. The Akt/NOS/mPTP pathway is involved in the microRNA-21-mediated protective effect of isoflurane.
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Dai, Qin-xue, Shan Li, Miao Ren, Xinlu Wu, Xin-yu Yao, Fei-hong Lin, Xu-qing Ni, Yun-chang Mo, and Jun-lu Wang. "Analgesia with 5' extracellular nucleotidase-mediated electroacupuncture for neuropathic pain." Arquivos de Neuro-Psiquiatria 80, no. 3 (March 2022): 289–95. http://dx.doi.org/10.1590/0004-282x-anp-2021-0149.
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ABSTRACT Background: Acupuncture is a treatment for neuropathic pain, but its mechanism remains unclear. Previous studies showed that analgesia was induced in rats with neuropathic pain when their spinal cord adenosine content increased after electroacupuncture (EA); however, the mechanism behind this electroacupuncture-induced increase has not been clarified. Objective: This study aimed to determine the role that ecto-5’-nucleotidase plays in EA-induced analgesia for neuropathic pain. Methods: We performed electroacupuncture at the Zusanli acupoint on the seventh day after establishing a rat model of neuropathic pain induced through chronic constriction injuries. We observed the mechanical withdrawal threshold and thermal pain threshold and detected the expression of ecto-5’-nucleotidase in the spinal cord using Western blot. Chronic constriction injury rat models were intraperitoneally injected with α,β-methyleneadenosine 5'-diphosphate, an ecto-5’-nucleotidase inhibitor, 30 min before electroacupuncture. The adenosine content of the spinal cord was detected using high-performance liquid chromatography. Lastly, the adenosine A1 receptor agonist N6-cyclopentyladenosine was intrathecally injected into the lumbar swelling of the rats, and the mechanical withdrawal and thermal pain thresholds were reevaluated. Results: Analgesia and increased ecto-5’-nucleotidase expression and adenosine content in the spinal cord were observed 1 h after electroacupuncture. α,β-methyleneadenosine 5'-diphosphate was able to inhibit upregulation of adenosine content and electroacupuncture-induced analgesia. After administration of N6-cyclopentyladenosine, electroacupuncture-induced analgesia was restored. Conclusions: Our results suggest that electroacupuncture at Zusanli can produce analgesia in chronic constriction injury rat models, possibly via the increased ecto-5’-nucleotidase expression induced through electroacupuncture, thus leading to increased adenosine expression in the spinal cord.
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Yu, Jin, Jianjiang Wu, Peng Xie, Yiliyaer Maimaitili, Jiang Wang, Zhengyuan Xia, Feng Gao, Xing Zhang, and Hong Zheng. "Sevoflurane postconditioning attenuates cardiomyocyte hypoxia/reoxygenation injury via restoring mitochondrial morphology." PeerJ 4 (November 3, 2016): e2659. http://dx.doi.org/10.7717/peerj.2659.
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Background Anesthetic postconditioning is a cellular protective approach whereby exposure to a volatile anesthetic renders a tissue more resistant to subsequent ischemic/reperfusion event. Sevoflurane postconditioning (SPostC) has been shown to exert cardioprotection against ischemia/reperfusion injury, but the underlying mechanism is unclear. We hypothesized that SPostC protects cardiomyocytes against hypoxia/reoxygenation (H/R) injury by maintaining/restoring mitochondrial morphological integrity, a critical determinant of cell fate. Methods Primary cultures of neonatal rat cardiomyocytes (NCMs) were subjected to H/R injury (3 h of hypoxia followed by 3 h reoxygenation). Intervention with SPostC (2.4% sevoflurane) was administered for 15 min upon the onset of reoxygenation. Cell viability, Lactate dehydrogenase (LDH) level, cell death, mitochondrial morphology, mitochondrial membrane potential and mitochondrial permeability transition pore (mPTP) opening were assessed after intervention. Mitochondrial fusion and fission regulating proteins (Drp1, Fis1, Mfn1, Mfn2 and Opa1) were assessed by immunofluorescence staining and western blotting was performed to determine the level of protein expression. Results Cardiomyocyte H/R injury resulted in significant increases in LDH release and cell death that were concomitant with reduced cell viability and reduced mitochondrial interconnectivity (mean area/perimeter ratio) and mitochondrial elongation, and with reduced mitochondrial membrane potential and increased mPTP opening. All the above changes were significantly attenuated by SPostC. Furthermore, H/R resulted in significant reductions in mitochondrial fusion proteins Mfn1, Mfn2 and Opa1 and significant enhancement of fission proteins Drp1 and Fis1. SPostC significantly enhanced Mfn2 and Opa1 and reduced Drp1, without significant impact on Mfn1 and Fis1. Conclusions Sevoflurane postconditioning attenuates cardiomyocytes hypoxia/reoxygenation injury (HRI) by restoring mitochondrial fusion/fission balance and morphology.
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Zhou, Tianqi, Chaodong Wu, Xutong Guan, Jialin Wang, Wen Zhu, and Bo Yuan. "Effect of Diagenetic Evolution and Hydrocarbon Charging on the Reservoir-Forming Process of the Jurassic Tight Sandstone in the Southern Junggar Basin, NW China." Energies 14, no. 23 (November 23, 2021): 7832. http://dx.doi.org/10.3390/en14237832.
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Deeply buried sandstones in the Jurassic, Toutunhe Formation, are a crucial exploration target in the Junggar Basin, NW China, whereas, reservoir-forming process of sandstones in the Toutunhe Formation remain unknown. Focused on the tight sandstone of the Toutunhe Formation, the impacts of diagenesis and hydrocarbon charging on sandstone reservoir-forming process were clarified based on the comprehensive analysis of sedimentary characteristics, petrography, petrophysical characteristics, and fluid inclusion analysis. Three diagenetic facies developed in the Toutunhe sandstone reservoirs, including carbonate cemented facies (CCF), matrix-caused tightly compacted facies (MTCF), and weakly diagenetic reformed facies (WDF). Except the WDF, the CCF and the MTCF entered the tight state in 18 Ma and 9 Ma, respectively. There was only one hydrocarbon emplacing event in sandstone reservoir of the Toutunhe Formation, charging in 13 Ma to 8 Ma. Meanwhile, the source rock started to expel hydrocarbons and buoyancy drove the hydrocarbon via the Aika fault belt to migrate into sandstone reservoirs in the Toutunhe Formation. During the end of the Neogene, the paleo-oil reservoir in the Toutunhe Formation was destructed and hydrocarbons migrated to the sandstone reservoirs in the Ziniquanzi Formation; some paleo-oil reservoirs survived in the WDF. The burial pattern and change of reservoir wettability were major controlling factors of the sandstone reservoir-forming process. The buried pattern of the Toutunhe Formation in the western section of the southern Junggar Basin was “slow and shallow burial at early stage and rapid and deep burial at late stage”. Hence, pore capillary pressure was extremely low due to limited diagenetic reformation (average pore capillary pressures were 0.26 MPa). At the same time, high content of chlorite coating increased the lipophilicity of reservoirs. Therefore, hydrocarbons preferably charged into the WDF with low matrix content (average 4.09%), high content of detrital quartz (average 28.75%), high content of chlorite films (average 2.2%), and lower pore capillary pressures (average 0.03 MPa). The above conditions were favorable for oil and gas enrichment.
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Yang, Yang, Yuanyuan Liu, Xi Chen, Jie Gong, Zhen Huang, Wei Wang, Yuanqi Shi, et al. "5-Aminolevulinic Acid-Mediated Sonodynamic Therapy Alleviates Atherosclerosis via Enhancing Efferocytosis and Facilitating a Shift in the Th1/Th2 Balance Toward Th2 Polarization." Cellular Physiology and Biochemistry 47, no. 1 (2018): 83–96. http://dx.doi.org/10.1159/000489751.
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Background/Aims: We and other groups have demonstrated that 5-aminolevulinic acid (ALA)-mediated sonodynamic therapy (ALA-SDT) induces macrophage and foam cell apoptosis and stabilizes atherosclerosis (AS) plaques in animal models. Lymphocytes also play vital roles in the development of AS. The primary purpose of the present study was to investigate the effects of ALA-SDT on T helper (Th) cell fate and function, Th subset differentiation, and atherosclerotic lesion stability. Methods: We utilized ALA-SDT on Western diet-fed apoE-/-mice in vivo and human Jurkat cells in vitro. Hematoxylin and eosin staining and TUNEL assays were used to evaluate the atherosclerotic plaque size and apoptosis within the atheroma. ALA induced cytotoxicity on cultured Jurkat cells was determined with CCK-8 assay. To address the mechanisms, levels of intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and mitochondrial permeability transition pore (MPTP) opening were evaluated by staining with fluorescent probes. Western blot analysis and confocal microscopy were used to analyze the protein levels of caspases, Bax and cytochrome c and the release of cytochrome c. Cell apoptosis and necrosis and phagocytosis were examined by flow cytometry. ELISAs and immunofluorescent staining were used to assess the corresponding cytokine levels and Th subset cell numbers within the atheroma. Results: Our studies revealed that ALA-SDT significantly enhanced CD4+ cell apoptosis and macrophage-mediated phagocytosis and hence reduced the necrotic core size. ALA-SDT activated the mitochondrial apoptotic signaling pathway with minimal necrosis in Jurkat cells. ALA-SDT inhibited the Th1 response and enhanced the Th2 response. These effects of ALA-SDT were mediated primarily through the generation of ROS. Conclusion: ALA-SDT alleviates AS by enhancing cytotoxic effects on Th cells, subsequently stimulating efferocytosis and facilitating a shift in the Th1/Th2 balance toward Th2 cells, a discovery that might help elucidate the mechanism underlying SDT as a potential treatment to prevent atherothrombotic events.
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Li, Nuo, Sina Qin, Lu Xie, Tao Qin, Yegui Yang, Wei Fang, and Meng-hua Chen. "Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial Preservation." Cellular Physiology and Biochemistry 48, no. 4 (2018): 1664–74. http://dx.doi.org/10.1159/000492289.
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Background/Aims: The anti-apoptotic effect of an increase in the extracellular concentration of potassium ([K+]) has been confirmed in vitro. However, it is not yet known whether elevated serum [K+] exerts a cerebroprotective effect in vivo. In this study, we aimed to explore the effect of elevated serum [K+] in a rat model of middle cerebral artery occlusion and reperfusion (MCAO/R). Methods: Rats subjected to 90-min MCAO received 2.5% KCL, 1.25% KCL, or a normal saline solution at a dose of 3.2 mL/kg at the onset of reperfusion. Rats that were subjected to vascular exposure and ligation without MCAO were defined as the Sham group. Serum [K+] was determined using a blood gas analyzer at 1 min after medicine administration. At 24 h post-reperfusion, rat brains were harvested and processed for 2% 2,3,5-triphenyltetrazolium chloride staining, terminal deoxynucleotidyl transferase-mediated 2′-deoxyuridine 5′-triphosphate-biotin nick end labeling staining, detection of caspase-3 and cleaved-caspase-3 by western blotting, detection of reactive oxygen species (ROS) by dihydroethidium staining, and observation of mitochondrial structure by electron microscopy. In addition, malondialdehyde (MDA), adenosine triphosphate (ATP), total superoxide dismutase (T-SOD), cytochrome C oxidase (COX) activity, and mitochondrial permeability transition pore (MPTP) opening were measured using detection kits. Results: The results showed that elevated serum [K+] decreased cerebral injury and apoptosis, reduced ROS and MDA levels and MPTP opening, increased ATP levels and cytochrome C oxidase activity, and improved mitochondrial ultrastructural changes, although there was no significant difference in T-SOD activity. Conclusion: These findings suggested that elevated serum [K+] could alleviate cerebral ischemia-reperfusion injury and the mechanism may be associated with the preservation of mitochondrial function.
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Chen, Xiaohui, Yujie Deng, Chuanzhong Huang, Yi Shi, Jianping Lu, Guibin Weng, Weifeng Zhu, Kunshou Zhu, Junqiang Chen, and Jiancheng Li. "RUNX3/H3K27me3 Co-Expression Defines a Better Prognosis in Surgically Resected Stage I and Postoperative Chemotherapy-Naive Non-Small-Cell Lung Cancer." Journal of Oncology 2022 (March 24, 2022): 1–23. http://dx.doi.org/10.1155/2022/5752263.
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The purpose of this study is to investigate the significance of RUNX3/H3K27me3 co-expression in surgically resected non-small-cell lung cancer (NSCLC) patients. Using tissue microarray (TMA), immunohistochemistry, fluorescent double immunostaining, and western blotting, 208 NSCLC and 5 benign pulmonary patients were studied of their expression of runt-related transcription factor 3 (RUNX3), trimethylated histone H3 at lysine 27 (H3K27me3), enhancer of zeste homolog 2 (EZH2), and Ki-67. Apoptotic index in cancerous tissue was evaluated via TdT-mediated dUTP-biotin nick end labeling (TUNEL). The correlation between clinicopathologic parameters and overall survival was determined by Cox regression and Kaplan–Meier survival estimates and log-rank test. GEPIA and KM plotter were used for validation of some survival analyses. As a result, together with other regular prognostic factors, RUNX3/H3K27me3 co-expression was found to be closely correlated with better prognosis in either pTNM-I or POCT-naive NSCLC patients, which might partially result from a higher cancerous apoptotic index. In conclusion, RUNX3/H3K27me3 co-expression defined some specific NSCLC population with better prognosis and longer OS and could probably be used as a biomarker in the prediction of better postoperative outcomes.
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Bernal-Ramírez, Judith, Christian Silva-Platas, Carlos Jerjes-Sánchez, Martín R. Ramos-González, Eduardo Vázquez-Garza, Héctor Chapoy-Villanueva, Alicia Ramírez-Rivera, Ángel Zarain-Herzberg, Noemi García, and Gerardo García-Rivas. "Resveratrol Prevents Right Ventricle Dysfunction, Calcium Mishandling, and Energetic Failure via SIRT3 Stimulation in Pulmonary Arterial Hypertension." Oxidative Medicine and Cellular Longevity 2021 (June 20, 2021): 1–15. http://dx.doi.org/10.1155/2021/9912434.
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Pulmonary arterial hypertension (PAH) is characterized by pulmonary vessel remodeling; however, its severity and impact on survival depend on right ventricular (RV) failure. Resveratrol (RES), a polyphenol found in red wine, exhibits cardioprotective effects on RV dysfunction in PAH. However, most literature has focused on RES protective effect on lung vasculature; recent finding indicates that RES has a cardioprotective effect independent of pulmonary arterial pressure on RV dysfunction, although the underlying mechanism in RV has not been determined. Therefore, this study is aimed at evaluating sirtuin-3 (SIRT3) modulation by RES in RV using a monocrotaline- (MC-) induced PAH rat model. Myocyte function was evaluated by confocal microscopy as cell contractility, calcium signaling, and mitochondrial membrane potential ( Δ Ψ m ); cell energetics was assessed by high-resolution respirometry, and western blot and immunoprecipitation evaluated posttranslational modifications. PAH significantly affects mitochondrial function in RV; PAH is prone to mitochondrial permeability transition pore (mPTP) opening, thus decreasing the mitochondrial membrane potential. The compromised cellular energetics affects cardiomyocyte function by decreasing sarco-endoplasmic reticulum Ca2+-ATPase (SERCA) activity and delaying myofilament unbinding, disrupting cell relaxation. RES partially protects mitochondrial integrity by deacetylating cyclophilin-D, a critical component of the mPTP, increasing SIRT3 expression and activity and preventing mPTP opening. The preserved energetic capability rescues cell relaxation by maintaining SERCA activity. Avoiding Ca2+ transient and cell contractility mismatch by preserving mitochondrial function describes, for the first time, impairment in excitation-contraction-energetics coupling in RV failure. These results highlight the importance of mitochondrial energetics and mPTP in PAH.
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Zhou, Xiaohui, Michael E. Konkel, and Douglas R. Call. "Type III secretion system 1 of Vibrio parahaemolyticus induces oncosis in both epithelial and monocytic cell lines." Microbiology 155, no. 3 (March 1, 2009): 837–51. http://dx.doi.org/10.1099/mic.0.024919-0.
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The Vibrio parahaemolyticus type III secretion system 1 (T3SS1) induces cytotoxicity in mammalian epithelial cells. We characterized the cell death phenotype in both epithelial (HeLa) and monocytic (U937) cell lines following infection with V. parahaemolyticus. Using a combination of the wild-type strain and gene knockouts, we confirmed that V. parahaemolyticus strain NY-4 was able to induce cell death in both cell lines via a T3SS1-dependent mechanism. Bacterial contact, but not internalization, was required for T3SS1-induced cytotoxicity. The mechanism of cell death involves formation of a pore structure on the surface of infected HeLa and U937 cells, as demonstrated by cellular swelling, uptake of cell membrane-impermeable dye and protection of cytotoxicity by osmoprotectant (PEG3350). Western blot analysis showed that poly ADP ribose polymerase (PARP) was not cleaved and remained in its full-length active form. This result was evident for seven different V. parahaemolyticus strains. V. parahaemolyticus-induced cytotoxicity was not inhibited by addition of the pan-caspase inhibitor carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone (Z-VAD-FMK) or the caspase-1 inhibitor N-acetyl-tyrosyl-valyl-alanyl-aspartyl-aldehyde (Ac-YVAD-CHO); thus, caspases were not involved in T3SS1-induced cytotoxicity. DNA fragmentation was not evident following infection and autophagic vacuoles were not observed after monodansylcadaverine staining. We conclude that T3SS1 of V. parahaemolyticus strain NY-4 induces a host cell death primarily via oncosis rather than apoptosis, pyroptosis or autophagy.
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Galymzhanov, B. "THE CONTINUITY IN THE WORKS OF MASHHUR ZHUSUP AND YUNUS EMRE." Bulletin of the Eurasian Humanities Institute, Philology Series, no. 3 (September 15, 2022): 144–53. http://dx.doi.org/10.55808/1999-4214.2022-3.14.
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The introduction of the paper covers the cognitive connections and similarities in the points of views of Yunus Emre, Mashkhur Zhussip and Qozha Akhmet Yassuyi. The poet Yunus Emre inferred the most reliable way to reach out to Allah is to love Allah, and it is not difficult to notice the essence of this view in the works of Mashkhur Zhussip who was a chronologist, historian, poet and ethnographer. Both of them gave a priority on the topics, such as life, death, wealth, fate and truth which human thinks upon. The paper discusses how they clearly and fairly stated human life and fate issues via elaborating mysteries in the essence of those topics. The paper presents both Mashkhur Zhussip and Yunus Emre called for people to strive for achieving perfection by managing their dissatisfaction through the instances in the main body of the paper. It justifies their creativity does not select a nation but focuses on all human values. The primary concept in the philosophy of Yunus Emre as well as Mashkhur Zussip is to love humans. Indeed we cannot say there are so many poets honouring and loving humans in the world literature. From their compositions, we are aware that these poets achieved to thinking level on humanism several centuries ago before the western purposed it. Yunus Emre and Mashkhur Zhussip considered values from all human values and positioned all are human despite their religion, language and ethnicity. Their works covering these views are thoroughly discussed in the main body of the paper. In the conclusion of the paper, we attempted to prove that the common thoughts met in all their poems are humanity, justice, acting by thinking and maintaining humanity and their effort were devoted to developing human spirit by giving examples from their poems.
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Wu, Ming-Feng, Ping-Chia Li, Chin-Chiu Chen, Su-Shin Ye, Chiang-Ting Chien, and Chia-Cherng Yu. "Cordyceps Sobolifera Extract Ameliorates Lipopolysaccharide-Induced Renal Dysfunction in the Rat." American Journal of Chinese Medicine 39, no. 03 (January 2011): 523–35. http://dx.doi.org/10.1142/s0192415x11009007.
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Cordyceps Sobolifera (CS), an economic traditional Chinese herb, may ameliorate nephrotoxicity-induced renal dysfunction in the rat via antioxidant, anti-apoptosis, and anti-autophagy mechanisms. We investigated the water extract of fermented whole broth of CS on lipopolysaccharide (LPS)-induced renal cell injury in vitro and in vivo. CS effect on LPS-induced epithelial Lilly pork kidney (PK1) and Madin-Darby canine kidney epithelial (MDCK) cell death was detected with MTT assay. Two-month treatment of CS effects on renal blood flow (RBF), glomerular filtration rate (GFR), plasma blood urea nitrogen, creatinine level and leukocytes (WBC) count were determined in the LPS-treated rats. We further examined the effects of CS supplement on renal tubular oxidative stress, endoplasmic reticulum stress, apoptosis and autophagy by Western blot analysis. LPS dose-dependently induced PK1 and MDCK cell death, which can be ameliorated by CS treatment. LPS significantly decreased RBF and GFR and increased blood leukocyte counts, plasma blood urea nitrogen and creatinine level in the rat after 24 hours of injury. LPS enhanced renal tubular ER stress, autophagy and apoptosis via by increase protein expressions of GRP78, caspase 12, Beclin-1 and Bax/Bcl-2 ratio. These findings are associated with the significant staining in renal proximal and distal tubular ED-1, GRP78, Beclin-1 autophagy, and TUNEL apoptosis in the LPS-treated kidneys. Two months of CS supplement significantly improved RBF, GFR and WBC values and reduced ED-1, GRP78, Beclin-1 autophagy and TUNEL apoptosis in the LPS-treated kidneys. Long-term CS treatment reduced LPS-induced stress responses and tissue damage possibly via blocking LPS-triggered signaling pathways.
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Goodwin, J. Y., A. C. Elmore, C. Salvinelli, and Mary R. Reidmeyer. "An optical method for characterizing carbon content in ceramic pot filters." Journal of Water and Health 15, no. 4 (May 26, 2017): 536–44. http://dx.doi.org/10.2166/wh.2017.049.
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Ceramic pot filter (CPF) technology is a relatively common means of household water treatment in developing areas, and performance characteristics of CPFs have been characterized using production CPFs, experimental CPFs fabricated in research laboratories, and ceramic disks intended to be CPF surrogates. There is evidence that CPF manufacturers do not always fire their products according to best practices and the result is incomplete combustion of the pore forming material and the creation of a carbon core in the final CPFs. Researchers seldom acknowledge the existence of potential existence of carbon cores, and at least one CPF producer has postulated that the carbon may be beneficial in terms of final water quality because of the presence of activated carbon in consumer filters marketed in the Western world. An initial step in characterizing the presence and impact of carbon cores is the characterization of those cores. An optical method which may be more viable to producers relative to off-site laboratory analysis of carbon content has been developed and verified. The use of the optical method is demonstrated via preliminary disinfection and flowrate studies, and the results of these studies indicate that the method may be of use in studying production kiln operation.
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Kudlacek, Patrick E., Jennifer L. Pluznick, Rong Ma, Babu Padanilam, and Steven C. Sansom. "Role of hβ1 in activation of human mesangial BK channels by cGMP kinase." American Journal of Physiology-Renal Physiology 285, no. 2 (August 2003): F289—F294. http://dx.doi.org/10.1152/ajprenal.00046.2003.
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In vascular smooth muscle and glomerular mesangial cells, relaxing agents such as nitric oxide and atrial natriuretic peptide activate large-conductance Ca2+-activated K+ channels (BK) via the cGMP kinase pathway. BK are composed of pore-forming α-subunits, encoded by the slopoke gene ( Slo), and one of four cell-specific accessory β-subunits (hβ1–4). We used patch-clamp analysis to determine the influence of hβ1, hβ2, and hβ4 on activation of human mesangial BK by cGMP kinase. We found that HEK 293 cells, coexpressing human (h) Sloα with either hβ1 or hβ2, contained single BK currents activated by db-cGMP in cell-attached patches. However, recombinant BK were not activated by db-cGMP when h Sloα was expressed alone or with hβ4. DNA-RNA hybridization revealed that mesangial cells contained mRNA for hβ1 but not hβ2 or hβ4. The BK response to db-cGMP was decreased when hβ1 antisense but not scrambled oligonucleotides were incorporated into mesangial cells. Western blot analysis showed that hβ1 antisense oligonucleotide inhibited the amount of hβ1-V5 fusion protein expressed in HEK 293 cells by ∼50%. These results show that mesangial cells contain hβ1, a BK accessory protein, which confers activation of BK by cGMP kinase.
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Penna, Claudia, Fabio Settanni, Francesca Tullio, Letizia Trovato, Pasquale Pagliaro, Giuseppe Alloatti, Ezio Ghigo, and Riccarda Granata. "GH-Releasing Hormone Induces Cardioprotection in Isolated Male Rat Heart via Activation of RISK and SAFE Pathways." Endocrinology 154, no. 4 (April 1, 2013): 1624–35. http://dx.doi.org/10.1210/en.2012-2064.
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Abstract GHRH stimulates GH synthesis and release from the pituitary and exerts direct effects in extrapituitary tissues. We have previously shown that pretreatment with GHRH reduces cardiomyocyte apoptosis and improves heart function in isolated rat hearts subjected to ischemia/reperfusion (I/R). Here, we determined whether GHRH given at reperfusion reduces myocardial reperfusion injury and investigated the molecular mechanisms involved in GHRH effects. Isolated rat hearts subjected to I/R were treated at the onset of reperfusion with: 1) GHRH; 2) GHRH+GHRH antagonist JV-1-36; 3) GHRH+mitochondrial ATP-dependent potassium channel inhibitor 5-hydroxydecanoate; 4) GHRH+mitochondrial permeability transition pore opener atractyloside; 5) GHRH+ phosphoinositide 3-kinase/Akt inhibitor Wortmannin (WM); and 6) GHRH+signal transducer and activator of transcription-3 inhibitor tyrphostin-AG490 (AG490). GHRH reduced infarct size at the end of reperfusion and reverted contractility dysfunction in I/R hearts. These effects were inhibited by either JV-1-36, 5-hydroxydecanoate, atractylosid, WM, or AG490. Western blot analysis on left ventricles showed GHRH-induced phosphorylation of either the reperfusion injury salvage kinases (RISK), phosphoinositide 3-kinase/Akt, ERK1/2, and glycogen synthase kinase-3β or signal transducer and activator of transcription-3, as part of the survivor activating factor enhancement (SAFE) pathway. GHRH-induced activation of RISK and SAFE pathways was blocked by JV-1-36, WM, and AG490. Furthermore, GHRH increased the phosphorylation of endothelial nitric oxide synthase and AMP-activated protein kinase and preserved postischemic nicotinamide adenine dinucleotide (NAD+) levels. These results suggest that GHRH protects the heart from I/R injury through receptor-mediated mechanisms, leading to activation of RISK and SAFE pathways, which converge on mitochondria and possibly on AMP-activated protein kinase.
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Yao, Huan, Qian Xie, Qingman He, Lei Zeng, Jing Long, Yuanyuan Gong, Xueping Li, et al. "Pretreatment with Panaxatriol Saponin Attenuates Mitochondrial Apoptosis and Oxidative Stress to Facilitate Treatment of Myocardial Ischemia-Reperfusion Injury via the Regulation of Keap1/Nrf2 Activity." Oxidative Medicine and Cellular Longevity 2022 (May 27, 2022): 1–20. http://dx.doi.org/10.1155/2022/9626703.
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Myocardial ischemia-reperfusion injury (MIRI) is a type of severe injury to the ischemic myocardium that can occur following recovery of blood flow, and for which, there is no effective treatment. Panaxatriol saponin (PTS), a major active component of P. notoginseng, has been used clinically to treat ischemia-related encephalopathy due to its antioxidant activity, but its effect on ischemic cardiomyopathy and underlying mechanism of action is still unclear. This study was performed to investigate the protective effect of PTS against MIRI and explore the potential underlying mechanisms. Hydrogen peroxide (H2O2) was used to stimulate cardiomyocytes, to mimic MIRI in vitro. Cell viability was tested using the CCK-8 method. The antioxidant activity of PTS in the H9c2 rat cardiomyocyte cell line was examined using 2 ′ ,7 ′ -dichlorodihydrofluorescein diacetate (DCFH-DA). The levels of superoxide dismutase-1 (SOD1), SOD2, and heme oxygenase (HO-1) were determined by Western blotting and/or immunofluorescence. The antiapoptotic effect of PTS was determined. In addition, mitochondrial permeability transition pore (mPTP) opening and mitochondrial membrane potential ( Δ Ψ m ) changes were assessed. Changes in Keap1/Nrf2 activation were evaluated by Western blotting analysis, molecular docking, and immunoprecipitation. An in vivo MIRI model was established in rats, and the myocardial infarct size was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Myocardial enzyme activities were determined by ELISA or biochemical analyses. Furthermore, changes in Nrf2 activation were evaluated, and the regulatory effect of PTS on cardiomyocyte apoptosis was examined using the Nrf2 blocker, ML385. The results showed that PTS ameliorated the cardiomyocyte injury induced by H2O2, characterized by increased cell viability, decreased reactive oxygen species (ROS) production, and promotion of SOD1, SOD2, and HO1 expression. PTS inhibited cardiomyocyte apoptosis in vivo and in vitro. PTS also reduced mPTP opening and stabilized Δ Ψ m in H9c2 cells. Molecular docking and immunoprecipitation study revealed that PTS can disrupt Keap1/Nrf2 interaction by directly blocking the binding site of Nrf2 in the Keap1 protein. In vivo, PTS decreased the area of myocardial infarction and attenuated pathological damage in ischemia-reperfusion (I/R) rats. In addition, the activities of myocardial injury markers were decreased by PTS. Finally, PTS regulated nuclear translocation of Nrf2, and ML385 blocked the therapeutic effect of PTS in vivo and in vitro. These results suggested that PTS has therapeutic potential for MIRI by targeting Keap1/Nrf2 activity.
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Wang, Xiaoping, Qianbin Sun, Qianqian Jiang, Yanyan Jiang, Yawen Zhang, Jing Cao, Linghui Lu, et al. "Cryptotanshinone Ameliorates Doxorubicin-Induced Cardiotoxicity by Targeting Akt-GSK-3β-mPTP Pathway In Vitro." Molecules 26, no. 5 (March 8, 2021): 1460. http://dx.doi.org/10.3390/molecules26051460.
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Cardiotoxicity is one of the main side effects of doxorubicin (Dox) treatment. Dox could induce oxidative stress, leading to an opening of the mitochondrial permeability transition pore (mPTP) and apoptosis in cardiomyocytes. Previous studies have shown that Cryptotanshinone (Cts) has potential cardioprotective effects, but its role in Dox-induced cardiotoxicity (DIC) remains unknown. A Dox-stimulated H9C2 cell model was established. The effects of Cts on cell viability, reactive oxygen species (ROS), superoxide ion accumulation, apoptosis and mitochondrial membrane potential (MMP) were evaluated. Expressions of proteins in Akt-GSK-3β pathway were detected by Western blot. An Akt inhibitor was applied to investigate the effects of Cts on the Akt-GSK-3β pathway. The effects of Cts on the binding of p-GSK-3β to ANT and the formation of the ANT-CypD complex were explored by immunoprecipitation assay. The results showed that Cts could increase cell viability, reduce ROS levels, inhibit apoptosis and protect mitochondrial membrane integrity. Cts increased phosphorylated levels of Akt and GSK-3β. After cells were co-treated with an Akt inhibitor, the effects of Cts were abolished. An immunoprecipitation assay showed that Cts significantly increased GSK-3β-ANT interaction and attenuated Dox-induced formation of the ANT-CypD complex, thereby inhibiting opening of the mPTP. In conclusion, Cts could ameliorate oxidative stress and apoptosis via the Akt-GSK-3β-mPTP pathway.
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Zheng, Xiufeng, Jinrong Wu, Qun Shao, Xuesong Li, Jiayuan Kou, Xing Zhu, Zhaoyu Zhong, et al. "Apoptosis of THP-1 Macrophages Induced by Pseudohypericin-Mediated Sonodynamic Therapy Through the Mitochondria-Caspase Pathway." Cellular Physiology and Biochemistry 38, no. 2 (2016): 545–57. http://dx.doi.org/10.1159/000438649.
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Background/Aims: Pseudohypericin (P-HY) and its congener hypericin are the major hydroxylated phenanthroperylenediones present in Hypericum species. Our previous study indicated that hypericin was able to function as a sonosensitizer. The potential use of P-HY as a sonosensitizer for sonodynamic therapy (SDT) requires further exploration. Thus, this study aimed to investigate the effects of P-HY-SDT on THP-1 macrophages. Methods: THP-1 macrophages were incubated with P-HY, and cell viability was measured using a CCK-8 assay. Fluorescence microscopy assessed the intracellular reactive oxygen species (ROS), mitochondrial membrane potential (∆Ψm) and mitochondrial permeability transition pore (mPTP) opening. Apoptotic and necrotic cell levels were measured by the flow cytometry analysis. Western blots were employed to assay BAX, Cytochrome C expression and apoptosis-related proteins. Results: P-HY-SDT induced THP-1 macrophage apoptosis. The levels of ROS were significantly increased in the SDT group, resulting in both mPTP opening and ∆Ψm loss, which led to apoptosis. In addition, the translocation of BAX, release of Cytochrome C and the upregulated expression of apoptosis-related proteins after P-HY-SDT were observed, all of which were reversed by N-acetyl cysteine (NAC). Conclusion: P-HY-SDT induced THP-1 macrophage apoptosis through the mitochondria-caspase pathway via ROS generation, the translocation of BAX and the release of Cytochrome C to regulate the mPTP opening.
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Jin, Qihui, Yanhong Jiang, Lizhong Fu, Yanqiu Zheng, Yuxia Ding, and Qian Liu. "Wenxin Granule Ameliorates Hypoxia/Reoxygenation-Induced Oxidative Stress in Mitochondria via the PKC-δ/NOX2/ROS Pathway in H9c2 Cells." Oxidative Medicine and Cellular Longevity 2020 (May 21, 2020): 1–16. http://dx.doi.org/10.1155/2020/3245483.
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Myocardial infarction and following reperfusion therapy-induced myocardial ischemia/reperfusion (I/R) injury have been recognized as an important subject of cardiovascular disease with high mortality. As the antiarrhythmic agent, Wenxin Granule (WXG) is widely used to arrhythmia and heart failure. In our pilot study, we found the antioxidative potential of WXG in the treatment of myocardial I/R. This study is aimed at investigating whether WXG could treat cardiomyocyte hypoxia/reoxygenation (H/R) injury by inhibiting oxidative stress in mitochondria. The H9c2 cardiomyocyte cell line was subject to H/R stimuli to mimic I/R injury in vitro. WXG was added to the culture medium 24 h before H/R exposing as pretreatment. Protein kinase C-δ (PKC-δ) inhibitor rottlerin or PKC-δ lentivirus vectors were conducted on H9c2 cells to downregulate or overexpress PKC-δ protein. Then, the cell viability, oxidative stress levels, intracellular and mitochondrial ROS levels, mitochondrial function, and apoptosis index were analyzed. In addition, PKC-δ protein expression in each group was verified by western blot analysis. Compared with the control group, the PKC-δ protein level was significantly increased in the H/R group, which was remarkably improved by WXG or rottlerin. PKC-δ lentivirus vector-mediated PKC-δ overexpression was not reduced by WXG. WXG significantly improved H/R-induced cell injury, lower levels of SOD and GSH/GSSG ratio, higher levels of MDA, intracellular and mitochondrial ROS content, mitochondrial membrane potential and ATP loss, mitochondrial permeability transition pore opening, NOX2 activation, cytochrome C release, Bax/Bcl-2 ratio and cleaved caspase-3 increasing, and cell apoptosis. Similar findings were obtained from rottlerin treatment. However, the protective effects of WXG were abolished by PKC-δ overexpression, indicating that PKC-δ was a potential target of WXG treatment. Our findings demonstrated a novel mechanism by which WXG attenuated oxidative stress and mitochondrial dysfunction of H9c2 cells induced by H/R stimulation via inhibitory regulation of PKC-δ/NOX2/ROS signaling.
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Chang, Alice S., Thomas F. Pedersen, and Ingrid L. Hendy. "Late Quaternary paleoproductivity history on the Vancouver Island margin, western Canada: a multiproxy geochemical studyThis article is one of a series of papers published in this Special Issue on the theme Polar Climate Stability Network." Canadian Journal of Earth Sciences 45, no. 11 (November 2008): 1283–97. http://dx.doi.org/10.1139/e08-038.
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Multiproxy analysis of a 38 m long sediment core recovered from the Vancouver Island margin (48.97°N, 127.04°W, water depth 1243 m) has yielded a millennial-scale history of upwelling and export production over the last ∼50 ka. Higher concentrations of marine organic carbon, opal, and trace Mo suggest that production was higher, and sedimentary pore waters more anoxic, during the warm Holocene, Bølling–Allerød, and interstadial events between 31 and 44 ka BP. Relatively lower production and higher inputs of terrigenous organic matter occurred during the last glacial (14.7–31 ka BP; Cordilleran ice sheet proximal to coring site at ∼19.5 ka BP) and from 44–50.4 ka BP. Enrichments in sedimentary δ15N during interstadial events are interpreted to reflect episodic delivery and upwelling of isotopically heavy nitrate to the surface waters and subsequent vectoring to the seafloor via settling planktonic detritus. Similar patterns are seen in southern California and other areas along the western margin of North America, implying that heavier nitrate generated by denitrification in the Eastern Tropical North Pacific has in the past been carried northward in the California Undercurrent at least as far as central Vancouver Island. This inference is consistent with modern hydrographic observations in the region. Comparison of the coherent Vancouver Island, Oregon, California, and northwest Mexico margin records with late Pleistocene climate history in Greenland reinforces the conclusion that a tight physical and biogeochemical coupling has existed for at least 50 ka between the North Atlantic and North American margin waters, including those off Vancouver Island.
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Bhattacharya, Sabyasachi, Tarunendu Mapder, Svetlana Fernandes, Chayan Roy, Jagannath Sarkar, Moidu Jameela Rameez, Subhrangshu Mandal, et al. "Sedimentation rate and organic matter dynamics shape microbiomes across a continental margin." Biogeosciences 18, no. 18 (September 23, 2021): 5203–22. http://dx.doi.org/10.5194/bg-18-5203-2021.
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Abstract. Marine sedimentation rate and bottom-water O2 concentration control organic carbon remineralization and sequestration across continental margins, but whether and how they shape microbiome architecture (the ultimate effector of all biogeochemical phenomena) across shelf and slope sediments is still unclear. Here we reveal distinct microbiome structures and functions, amidst comparable pore fluid chemistries, along 300 cm sediment horizons underlying the seasonal (shallow coastal; water depth: 31 m) and perennial (deep sea; water depths: 530 and 580 m) oxygen minimum zones (OMZs) of the Arabian Sea, situated across the western Indian margin. The sedimentary geomicrobiology was elucidated by analyzing metagenomes, metatranscriptomes, enrichment cultures, and depositional rates measured via radiocarbon and lead excess dating; the findings were then evaluated in light of the other geochemical data available for the cores. Along the perennial-OMZ sediment cores, microbial communities were dominated by Gammaproteobacteria and Alphaproteobacteria, but in the seasonal-OMZ core communities were dominated by Euryarchaeota and Firmicutes. As a perennial-OMZ signature, a cryptic methane production–consumption cycle was found to operate near the sediment surface, within the sulfate reduction zone; overall diversity, as well as the relative abundances of anaerobes requiring simple fatty acids (methanogens, anaerobic methane oxidizers, sulfate reducers, and acetogens), peaked in the topmost sediment layer and then declined via synchronized fluctuations until the sulfate–methane transition zone was reached. The microbiome profile was completely reversed in the seasonal-OMZ sediment horizon. In the perennial-OMZ sediments, deposited organic carbon was higher in concentration and rich in marine components that degrade readily to simple fatty acids; simultaneously, lower sedimentation rate afforded higher O2 exposure time for organic matter degradation despite perennial hypoxia in the bottom water. The resultant abundance of reduced carbon substrates eventually sustained multiple inter-competing microbial processes in the upper sediment layers. The entire geomicrobial scenario was opposite in the sediments of the seasonal OMZ. These findings create a microbiological baseline for understanding carbon–sulfur cycling in distinct depositional settings and water column oxygenation regimes across the continental margins.
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Kazi, Rafi, Waitman Kurt Aumann, Pritha Bagchi, Donald Tope, and Daniel S. Wechsler. "Establishing the Role of EPS15, DVL2 and Cortactin in CALM-AF10 Leukemogenesis." Blood 138, Supplement 1 (November 5, 2021): 3312. http://dx.doi.org/10.1182/blood-2021-152644.
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Abstract Background: Leukemia is the most common type of childhood cancer. Although the prognosis for many pediatric leukemias has improved, leukemias associated with the t(10;11) CALM-AF10 translocation remain difficult to treat. CALM-AF10 leukemias account for ~5-10% of childhood T-cell acute lymphoblastic leukemia (T-ALL)as well as a subset of acute myeloid leukemia (AML). CALM-AF10 leukemias exhibit increased expression of proleukemic HOXA genes, but relatively little is known about the cellular mechanisms that drive CALM-AF10 leukemogenesis. Our laboratory has demonstrated that the CALM protein contains a nuclear export signal (NES) that is critical for CALM-AF10-dependent leukemogenesis. The NES interacts with the CRM1/XPO1 nuclear export receptor, which shuttles proteins from the nucleus to the cytoplasm through the nuclear pore complex. We have shown that transcriptional activation of HOXA genes by CALM-AF10 is dependent on its interaction with CRM1. Importantly, CRM1 does not contain a recognized DNA binding domain, and it is not currently understood how the CALM-AF10/CRM1 complex interacts with regulatory regions of HOXA genes. To identify proteins that mediate the interaction between the CALM-AF10/CRM1 complex and DNA, we took advantage of a proximity-based labeling approach using BioID2, a second-generation biotin ligase. When fused to a protein of interest and in the presence of biotin, BioID2 biotinylates proteins in close proximity to the ligase. These biotinylated proteins can then be identified by mass spectrometry (MS). Methods: We prepared an expression plasmid in which BioID2 was cloned in-frame with CALM-AF10. Human Embryonic Kidney 293 (HEK293) cells were transiently transfected with BioID2-CALM-AF10 and grown in the presence or absence of biotin. MS was performed to identify candidate interacting proteins. We validated direct interactions of candidate proteins with CALM-AF10 using co-immunoprecipitation experiments in HEK293 cells transfected with a CALM-AF10 plasmid. We confirmed that candidate proteins are present in murine CALM-AF10 leukemia cells via Western blotting. In order to efficiently knockout (KO) candidate proteins, we have generated a human U937 cell line (which harbors a t(10;11) CALM-AF10 translocation) with a stable incorporated Cas9. To assess whether KO of EPS15, DVL2 or CTTN affects HOXA5 expression, we performed RT-qPCR in U937-Cas9 cells lines with confirmed KO. Results: We carried out three independent transfections/MS experiments, which identified 71, 95 and 61 proteins, respectively. Of the proteins identified, 12 candidates were common to all three experiments . Importantly, we identified Disruptor Of Telomeric silencing 1-Like (DOT1L), a protein known to interact with AF10, and Nuclear pore complex protein 214 (NUP214), a protein that interacts with CRM1 and that is involved in leukemogenic translocations. We chose EPS15, DVL2 and CTTN for further study, as each of these proteins plays a role in leukemogenesis. We performed initial validation of direct interactions via co-immunoprecipitation and found that all three proteins co-precipitate with CALM-AF10. Western blotting showed that all three proteins are expressed in a murine CALM-AF10 leukemia cell line. We effectively knocked out EPS15 protein expression in U937 cells, and showed that HOXA5 expression is reduced in the setting of EPS15 knockout. Conclusion: We used biotin ligase-dependent proximity-based labeling to identify candidate proteins that potentially interact with the CALM-AF10 fusion protein. Our identification of DOT1L validates the approach, since DOT1L is known to interact with CALM-AF10. We have started to investigate three candidate proteins - EPS15, DVL2 and CTTN - all of which are involved in leukemogenic transformation. We have shown that EPS15, DVL2 and CTTN are expressed in murine CALM-AF10 leukemia cells and directly interact with the CALM-AF10 fusion protein. Knockout of EPS15 in U937 cells results in decreased HOXA5 expression, suggesting the importance of EPS15 in CALM-AF10 leukemogenesis. Evaluation of the roles of these proteins in leukemogenesis may lead to identification of novel pathways involved in CALM-AF10 leukemogenesis. Disclosures No relevant conflicts of interest to declare.
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Schroder, Elizabeth, Janos Magyar, Don Burgess, Douglas Andres, and Jonathan Satin. "Chronic verapamil treatment remodels ICa,L in mouse ventricle." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 4 (April 2007): H1906—H1916. http://dx.doi.org/10.1152/ajpheart.00793.2006.
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In this study we tested the hypothesis that ventricular homeostasis of L-type Ca2+ current ( ICa,L) minimally involves regulation of the main pore-forming α-subunit (CaV1.2) and auxiliary proteins that serve as positive or negative regulators of ICa,L. We treated animals for 24 h with verapamil (Ver, 3.6 mg·kg−1·day−1), isoproterenol (Iso, 30 mg·kg−1·day−1), or Iso + Ver via osmotic minipumps. To test for alterations of Ca2+ channel complex components we performed real-time PCR and Western blot analysis on ventricle. In addition, cardiac myocytes (CMs) were dispersed and current was recorded in the whole cell configuration to evaluate ICa,L. Surprisingly, 24- to 48-h Ver increased CaV1.2 mRNA and protein and ICa,L current (Ver 11 ± 1pA/pF vs. control 7 ± 0.5pA/pF; P < 0.01). ICa,L from CMs in Ver mice showed no change in whole cell capacitance. To examine the in vivo effects of a physiologically relevant Ca2+ channel agonist, we treated mice with Iso. Twenty-four-hour Iso infusion increased heart rate; CaV1.2- and CaVβ2 mRNA levels were constant, but the Ca2+ channel subunit mRNA Rem was increased twofold. Cells isolated from 24-h Iso hearts showed no change in basal ICa,L density and diminished responsiveness to acute 1 μM Iso. To further examine the homeostatic regulation of the Ca2+ channel, we treated animals for 24 h with Iso + Ver. The influence of Iso + Ver was similar that of to Iso alone on Ca2+ channel mRNAs and ICa,L, with the exception that it prevented the increase in Rem seen with Iso treatment. Long-term Ca2+ channel blockade induces an increase of CaV1.2 mRNA and protein and significantly increases ICa,L.
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Stadnicka, Anna, Jasna Marinovic, Martin Bienengraeber, and Zeljko J. Bosnjak. "Impact of In Vivo Preconditioning by Isoflurane on Adenosine Triphosphate–sensitive Potassium Channels in the Rat Heart." Anesthesiology 104, no. 3 (March 1, 2006): 503–10. http://dx.doi.org/10.1097/00000542-200603000-00018.
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Background The early memory of anesthetic-induced preconditioning (APC) is a period when myocardial protection continues even after removal of the anesthetic. Because adenosine triphosphate-sensitive potassium (KATP) channels are important mediators of APC, the authors investigated the hypothesis that the memory involves channel priming by isoflurane via a long-term modulation of the sensitivity to intracellular adenosine nucleotides. Methods Ventricular cardiomyocytes were obtained from the rat hearts after 30 min in vivo APC with 1.4% isoflurane and from control non-APC rat hearts. Whole cell and excised inside-out patch clamp techniques were used to study the sarcolemmal KATP channel. Membrane expression of KATP channel proteins, the pore-forming inward rectifier Kir6.2, and the regulatory sulfonylurea receptor SUR2A were assessed in APC and non-APC hearts by Western blotting. Results Activation of whole cell KATP current by isoflurane was enhanced after in vivo APC. At the single-channel level, this was paralleled by a 12-fold decrease in adenosine 5'-triphosphate sensitivity and a 3-fold decrease in adenosine 5'-diphosphate sensitivity, without changing the probability of channel opening or single-channel conductance. The membrane expression of Kir6.2 and SUR2A subunits was not altered by in vivo APC. A direct in vitro application of isoflurane to excised membrane patches increased the channel open probability and produced a 4-fold decrease in adenosine 5'-triphosphate sensitivity only of channels in non-APC myocytes. Conclusions In vivo APC by isoflurane decreases sensitivity of the sarcolemmal KATP channel to inhibition by adenosine 5'-triphosphate and decreases adenosine 5'-diphosphate sensitivity. These effects persist even after discontinuation of the anesthetic, suggesting a possible novel factor that may contribute to the mechanism of early memory of APC.
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Kirkegaard, Signe Skyum, Ian Henry Lambert, Steen Gammeltoft, and Else Kay Hoffmann. "Activation of the TASK-2 channel after cell swelling is dependent on tyrosine phosphorylation." American Journal of Physiology-Cell Physiology 299, no. 4 (October 2010): C844—C853. http://dx.doi.org/10.1152/ajpcell.00024.2010.
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The swelling-activated K+ currents ( IK,vol) in Ehrlich ascites tumor cells (EATC) has been reported to be through the two-pore domain (K2p), TWIK-related acid-sensitive K+ channel 2 (TASK-2). The regulatory volume decrease (RVD), following hypotonic exposure in EATC, is rate limited by IK,vol indicating that inhibition of RVD reflects inhibition of TASK-2. We find that in EATC the tyrosine kinase inhibitor genistein inhibits RVD by 90%, and that the tyrosine phosphatase inhibitor monoperoxo(picolinato)-oxo-vanadate(V) [mpV(pic)] shifted the volume set point for inactivation of the channel to a lower cell volume. Swelling-activated K+ efflux was impaired by genistein and the Src kinase family inhibitor 4-amino-5-(4-chloro-phenyl)-7-( t-butyl)pyrazolo[3,4- d]pyrimidine (PP2) and enhanced by the tyrosine phosphatase inhibitor mpV(pic). With the use of the TASK-2 inhibitor clofilium, it is demonstrated that mpV(pic) increased the volume-sensitive part of the K+ efflux 1.3 times. To exclude K+ efflux via a KCl cotransporter, cellular Cl− was substituted with NO3−. Also under these conditions K+ efflux was completely blocked by genistein. Thus tyrosine kinases seem to be involved in the activation of the volume-sensitive K+ channel, whereas tyrosine phosphatases appears to be involved in inactivation of the channel. Overexpressing TASK-2 in human embryonic kidney (HEK)-293 cells increased the RVD rate and reduced the volume set point. TASK-2 has tyrosine sites, and precipitation of TASK-2 together with Western blotting and antibodies against phosphotyrosines revealed a cell swelling-induced, time-dependent tyrosine phosphorylation of the channel. Even though we found an inhibiting effect of PP2 on RVD, neither Src nor the focal adhesion kinase (FAK) seem to be involved. Inhibitors of the epidermal growth factor receptor tyrosine kinases had no effect on RVD, whereas the Janus kinase (JAK) inhibitor cucurbitacin inhibited the RVD by 40%. It is suggested that the cytokine receptor-coupled JAK/STAT pathway is upstream of the swelling-induced phosphorylation and activation of TASK-2 in EATC.