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Find video protocols related to scientific articles indexed in Pubmed.
Potential Effects of Calcium Binding Protein S100A12 on Severity Evaluation and Curative Effect of Severe Acute Pancreatitis.
Inflammation
PUBLISHED: 10-01-2014
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Severe acute pancreatitis is a life threatening disease with a high rate of mortality, but its treatments are still controversial. The purpose of this study is to investigate the potential effects of calcium binding protein S100A12 on severity evaluation and curative effect of severe acute pancreatitis induced by caerulein and lipopolysaccharide in mice. Intraperitoneal injection of 50 ?g/kg caerulein for seven times (every interval time was an hour) and intraperitoneal injection of 10 mg/kg lipopolysaccharide for once to establish acute pancreatitis mice models. One hundred sixty specific pathogen-free imprinting control region (ICR) female mice were randomly divided into the control group (group A, normal saline), the mild group (group B, caerulein), the severe group (group C, caerulein + lipopolysaccharide), and the intervention group (group D, S100A12 recombinant antibodies + caerulein + lipopolysaccharide); each group had 40 mice. We sampled the blood at 8, 12, and 24 h after the beginning of building animal models. In each period of time, we respectively detected the serum S100A12, amylase (AMY), C-reactive protein (CRP), interleukin (IL-1?, IL-6), and tumor necrosis factor (TNF-?) levels. In addition, we observed and scored the pancreas and lungs histopathology of the mice. In each same period of time compared with group C, serum AMY, CRP, IL-1?, IL-6, TNF-? levels of group D were significantly decreased (p?
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Genome-wide association study in Chinese identifies novel loci for blood pressure and hypertension.
Hum. Mol. Genet.
PUBLISHED: 09-23-2014
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Hypertension is a common disorder and the leading risk factor for cardiovascular disease and premature deaths worldwide. Genome-wide association studies (GWASs) in the European population have identified multiple chromosomal regions associated with blood pressure, and the identified loci altogether explain only a small fraction of the variance for blood pressure. The differences in environmental exposures and genetic background between Chinese and European populations might suggest potential different pathways of blood pressure regulation. To identify novel genetic variants affecting blood pressure variation, we conducted a meta-analysis of GWASs of blood pressure and hypertension in 11 816 subjects followed by replication studies including 69 146 additional individuals. We identified genome-wide significant (P < 5.0 × 10(-8)) associations with blood pressure, which included variants at three new loci (CACNA1D, CYP21A2, and MED13L) and a newly discovered variant near SLC4A7. We also replicated 14 previously reported loci, 8 (CASZ1, MOV10, FGF5, CYP17A1, SOX6, ATP2B1, ALDH2, and JAG1) at genome-wide significance, and 6 (FIGN, ULK4, GUCY1A3, HFE, TBX3-TBX5, and TBX3) at a suggestive level of P = 1.81 × 10(-3) to 5.16 × 10(-8). These findings provide new mechanistic insights into the regulation of blood pressure and potential targets for treatments.
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Abiotic stress resistance, a novel moonlighting function of ribosomal protein RPL44 in the halophilic fungus Aspergillus glaucus.
Appl. Environ. Microbiol.
PUBLISHED: 05-09-2014
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Ribosomal proteins are highly conserved components of basal cellular organelles, primarily involved in the translation of mRNA leading to protein synthesis. However, certain ribosomal proteins moonlight in the development and differentiation of organisms. In this study, the ribosomal protein L44 (RPL44), associated with salt resistance, was screened from the halophilic fungus Aspergillus glaucus (AgRPL44), and its activity was investigated in Saccharomyces cerevisiae and Nicotiana tabacum. Sequence alignment revealed that AgRPL44 is one of the proteins of the large ribosomal subunit 60S. Expression of AgRPL44 was upregulated via treatment with salt, sorbitol, or heavy metals to demonstrate its response to osmotic stress. A homologous sequence from the model fungus Magnaporthe oryzae, MoRPL44, was cloned and compared with AgRPL44 in a yeast expression system. The results indicated that yeast cells with overexpressed AgRPL44 were more resistant to salt, drought, and heavy metals than were yeast cells expressing MoRPL44 at a similar level of stress. When AgRPL44 was introduced into M. oryzae, the transformants displayed obviously enhanced tolerance to salt and drought, indicating the potential value of AgRPL44 for genetic applications. To verify the value of its application in plants, tobacco was transformed with AgRPL44, and the results were similar. Taken together, we conclude that AgRPL44 supports abiotic stress resistance and may have value for genetic application.
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Roles of DgBRC1 in regulation of lateral branching in chrysanthemum (Dendranthema ×grandiflora cv. Jinba).
PLoS ONE
PUBLISHED: 01-01-2013
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The diverse plasticity of plant architecture is largely determined by shoot branching. Shoot branching is an event regulated by multiple environmental, developmental and hormonal stimuli through triggering lateral bud response. After perceiving these signals, the lateral buds will respond and make a decision on whether to grow out. TCP transcriptional factors, BRC1/TB1/FC1, were previously proven to be involved in local inhibition of shoot branching in Arabidopsis, pea, tomato, maize and rice. To investigate the function of BRC1, we isolated the BRC1 homolog from chrysanthemum. There were two transcripts of DgBRC1 coming from two alleles in one locus, both of which complemented the multiple branches phenotype of Arabidopsis brc1-1, indicating that both are functionally conserved. DgBRC1 was mainly expressed in dormant axillary buds, and down-regulated at the bud activation stage, and up-regulated by higher planting densities. DgBRC1 transcripts could respond to apical auxin supply and polar auxin transport. Moreover, we found that the acropetal cytokinin stream promoted branch outgrowth whether or not apical auxin was present. Basipetal cytokinin promoted outgrowth of branches in the absence of apical auxin, while strengthening the inhibitory effects on lower buds in the presence of apical auxin. The influence of auxin and strigolactons (SLs) on the production of cytokinin was investigated, we found that auxin locally down-regulated biosynthesis of cytokinin in nodes, SLs also down-regulated the biosynthesis of cytokinin, the interactions among these phytohormones need further investigation.
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Expression of active protein phosphatase 1 inhibitor-1 attenuates chronic beta-agonist-induced cardiac apoptosis.
Basic Res. Cardiol.
PUBLISHED: 02-04-2010
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Cardiac apoptosis has been considered an important contributing factor to heart failure. Several subcellular mechanisms, including increased protein phosphatase 1 activity, have been suggested to induce apoptosis. Protein phosphatase 1 is regulated by an endogenous inhibitor-1 (I-1) that is activated upon phosphorylation at threonine 35 via protein kinase A. Here, we tested whether cardiac-specific overexpression of a constitutively active (T35D, AA 1-65) inhibitor-1 (I-1c), could also affect cardiac apoptosis and heart failure progression induced by prolonged beta-adrenergic stimulation. We found that either acute or chronic expression of I-1c reduced isoproterenol (ISO)-induced apoptosis assessed by nuclear condensation, TUNEL staining and DNA fragmentation. The beneficial effects of I-1c were associated with increased expression of the anti-apoptotic protein Bcl-2, decreased expression of the pro-apoptotic protein Bax and reduced levels of active caspases as well as increased activation of ERK. These findings suggest that mitochondrial signaling and ERK activation may be involved in the I-1c cardioprotective effects against apoptosis induced by prolonged beta-adrenergic stimulation.
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Salt-induced expression of genes related to Na(+)/K(+) and ROS homeostasis in leaves of salt-resistant and salt-sensitive poplar species.
Plant Mol. Biol.
PUBLISHED: 01-30-2010
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Using the Affymetrix poplar genome array, we explored the leaf transcriptome of salt-tolerant Populus euphratica Oliv. and salt-sensitive P. popularis 35-44 (P. popularis) under control and saline conditions. Our objective was to clarify the genomic differences in regulating K(+)/Na(+) and reactive oxygen species (ROS) homeostasis between the two species. Compared to P. popularis, salt-tolerant P. euphratica responses to salinity involved induction of a relatively larger number of probesets after short-term (ST) exposure to 150 mM NaCl (24 h) and relatively fewer probesets after a long-term (LT) exposure to salinity (200 mM NaCl, 28 days). Compared to P. popularis, leaves of the control P. euphratica plants exhibited a higher transcript abundance of genes related to Na(+)/H(+) antiport (Na(+)/H(+) antiporters, H(+) pumps) and K(+) uptake and transport. Notably, the expression of these genes did not decrease (with a few exceptions) during salt treatment. Regarding ROS homeostasis, P. euphratica exhibited rapid up-regulation of a variety of antioxidant enzymes after exposure to ST salinity, indicating a rapid adaptive response to salt stress. However, the effect of NaCl on transcription in P. popularis leaves was more pronounced after exposure to prolonged salinity. LT-stressed P. popularis up-regulated some genes mediating K(+)/Na(+) homeostasis but decreased transcription of main scavengers of superoxide radicals and H(2)O(2) except for some isoforms of a few scavengers. Mineral and ROS analyses show that NaCl induced a marked increase of leaf Na(+) and H(2)O(2) in LT-stressed plants of the two species and the effects were even more pronounced in the salt-sensitive poplar. We place the transcription results in the context of our physiological measurements to infer some implications of NaCl-induced alterations in gene expression related to K(+)/Na(+) and ROS homeostasis.
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Protection of peroxiredoxin II on oxidative stress-induced cardiomyocyte death and apoptosis.
Basic Res. Cardiol.
PUBLISHED: 07-30-2009
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Peroxiredoxin II, a cytosolic isoform of the antioxidant enzyme family, has been implicated in cancer-associated cell death and apoptosis, but its functional role in the heart remains to be elucidated. Interestingly, the expression levels of peroxiredoxin II were decreased in mouse hearts upon ischemia-reperfusion, while they were elevated in two genetically modified hyperdynamic hearts with phospholamban ablation or protein phosphatase 1 inhibitor 1 overexpression. To delineate the functional significance of altered peroxiredoxin II expression, adenoviruses encoding sense or antisense peroxiredoxin II were generated; cardiomyocytes were infected, and then subjected to H(2)O(2) treatment to mimic oxidative stress-induced cell death and apoptosis. H(2)O(2) stimulation resulted in a significant decrease of endogenous peroxiredoxin II expression, along with reduced cell viability in control cells. However, overexpression of peroxiredoxin II significantly protected from H(2)O(2)-induced apoptosis and necrosis, while downregulation of this enzyme promoted the detrimental effects of oxidative stress in cardiomyocytes. The beneficial effects of peroxiredoxin II were associated with increased Bcl-2 expression, decreased expression of Bax and attenuated activity of caspases 3, 9 and 12. Furthermore, there were no significant alterations in the expression levels of the other five isoforms of peroxiredoxin, as well as active catalase or glutathione peroxidase-1 after ischemia-reperfusion or H(2)O(2) treatment. These findings suggest that peroxiredoxin II may be a unique antioxidant in the cardiac system and may represent a potential target for cardiac protection from oxidative stress-induced injury.
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Calcium mediates root K+/Na+ homeostasis in poplar species differing in salt tolerance.
Tree Physiol.
PUBLISHED: 07-28-2009
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Using the non-invasively ion-selective microelectrode technique, flux profiles of K(+), Na(+) and H(+) in mature roots and apical regions, and the effects of Ca(2+) on ion fluxes were investigated in salt-tolerant poplar species, Populus euphratica Oliver and salt-sensitive Populus simonii x (P. pyramidalis + Salix matsudana) (Populus popularis 35-44, P. popularis). Compared to P. popularis, P. euphratica roots exhibited a greater capacity to retain K(+) after exposure to a salt shock (SS, 100 mM NaCl) and a long-term (LT) salinity (50 mM NaCl, 3 weeks). Salt shock-induced K(+) efflux in the two species was markedly restricted by K(+) channel blocker, tetraethylammonium chloride, but enhanced by sodium orthovanadate, the inhibitor of plasma membrane (PM) H(+)-ATPase, suggesting that the K(+) efflux is mediated by depolarization-activated (DA) channels, e.g., KORCs (outward rectifying K(+) channels) and NSCCs (non-selective cation channels). Populus euphratica roots were more effective to exclude Na(+) than P. popularis in an LT experiment, resulting from the Na(+)/H(+) antiport across the PM. Moreover, pharmacological evidence implies that the greater ability to control K(+)/Na(+) homeostasis in salinized P. euphratica roots is associated with the higher H(+)-pumping activity, which provides an electrochemical H(+) gradient for Na(+)/H(+) exchange and simultaneously decreases the NaCl-induced depolarization of PM, thus reducing Na(+) influx via NSCCs and K(+) efflux through DA-KORCs and DA-NSCCs. Ca(2+) application markedly limited salt-induced K(+) efflux but enhanced the apparent Na(+) efflux, thus enabling the two species, especially the salt-sensitive poplar, to retain K(+)/Na(+) homeostasis in roots exposed to prolonged NaCl treatment.
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NaCl-induced alternations of cellular and tissue ion fluxes in roots of salt-resistant and salt-sensitive poplar species.
Plant Physiol.
PUBLISHED: 05-15-2009
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Using the scanning ion-selective electrode technique, fluxes of H+, Na+, and Cl- were investigated in roots and derived protoplasts of salt-tolerant Populus euphratica and salt-sensitive Populus popularis 35-44 (P. popularis). Compared to P. popularis, P. euphratica roots exhibited a higher capacity to extrude Na+ after a short-term exposure to 50 mM NaCl (24 h) and a long term in a saline environment of 100 mM NaCl (15 d). Root protoplasts, isolated from the long-term-stressed P. euphratica roots, had an enhanced Na+ efflux and a correspondingly increased H+ influx, especially at an acidic pH of 5.5. However, the NaCl-induced Na+/H+ exchange in root tissues and cells was inhibited by amiloride (a Na+/H+ antiporter inhibitor) or sodium orthovanadate (a plasma membrane H+-ATPase inhibitor). These results indicate that the Na+ extrusion in stressed P. euphratica roots is the result of an active Na+/H+ antiport across the plasma membrane. In comparison, the Na+/H+ antiport system in salt-stressed P. popularis roots was insufficient to exclude Na+ at both the tissue and cellular levels. Moreover, salt-treated P. euphratica roots retained a higher capacity for Cl- exclusion than P. popularis, especially during a long term in high salinity. The pattern of NaCl-induced fluxes of H+, Na+, and Cl- differs from that caused by isomotic mannitol in P. euphratica roots, suggesting that NaCl-induced alternations of root ion fluxes are mainly the result of ion-specific effects.
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The human G147D-protein phosphatase 1 inhibitor-1 polymorphism is not associated with altered clinical characteristics in heart failure.
Cardiology
PUBLISHED: 04-30-2009
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A human protein phosphatase inhibitor-1 polymorphism, G147D (c.440G>A, p.147G>D), has been previously demonstrated to blunt the contractile responses of cardiomyocytes to beta-adrenergic agonists. The present study sought to examine whether the G147D inhibitor-1 polymorphism may be associated with specific clinical characteristics of heart failure carriers.
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Inducible expression of active protein phosphatase-1 inhibitor-1 enhances basal cardiac function and protects against ischemia/reperfusion injury.
Circ. Res.
PUBLISHED: 03-19-2009
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Ischemic heart disease, which remains the leading cause of morbidity and mortality in the Western world, is invariably characterized by impaired cardiac function and disturbed Ca(2+) homeostasis. Because enhanced inhibitor-1 (I-1) activity has been suggested to preserve Ca(2+) cycling, we sought to define whether increases in I-1 activity in the adult heart may ameliorate contractile dysfunction and cellular injury in the face of an ischemic insult. To this end, we generated an inducible transgenic mouse model that enabled temporally controlled expression of active I-1 (T35D). Active I-1 expression in the adult heart elicited significant enhancement of contractile function, associated with preferential phospholamban phosphorylation and enhanced sarcoplasmic reticulum Ca(2+)-transport. Further phosphoproteomic analysis revealed alterations in proteins associated with energy production and protein synthesis, possibly to support the increased metabolic demands of the hyperdynamic hearts. Importantly, on ischemia/reperfusion-induced injury, active I-1 expression augmented contractile function and recovery. Further examination revealed that the infarct region and apoptotic as well as necrotic injuries were significantly attenuated by enhanced I-1 activity. These cardioprotective effects were associated with suppression of the endoplasmic reticulum stress response. The present findings indicate that increased I-1 activity in the adult heart enhances Ca(2+) cycling and improves mechanical recovery, as well as cell survival after an ischemic insult, suggesting that active I-1 may represent a potential therapeutic strategy in myocardial infarction.
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Partial downregulation of junctin enhances cardiac calcium cycling without eliciting ventricular arrhythmias in mice.
Am. J. Physiol. Heart Circ. Physiol.
PUBLISHED: 03-13-2009
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Human failing hearts exhibit significant decreases in junctin expression levels with almost nondetectable levels, which may be associated with premature death, induced by lethal cardiac arrhythmias, based on mouse models. However, the specific contribution of junctin to the delayed afterdepolarizations has been difficult to delineate in the phase of increased Na(+)-Ca(2+) exchanger activity accompanying junctin ablation. Thus we characterized the heterozygous junctin-deficient hearts, which expressed 54% of junctin levels and similar increases in Na(+)-Ca(2+) exchanger activity, as the null model. Cardiac contractile parameters, Ca(2+) transients, and sarcoplasmic reticulum Ca(2+) content were significantly increased in junctin heterozygous hearts, although they did not reach the levels of null hearts. However, Ca(2+) spark properties were not altered in heterozygous cardiomyocytes, compared with wild-types, and there were no aftercontractions elicited by the increased frequency of stimulation in the presence of isoproterenol, unlike the junctin-deficient cells. Furthermore, heterozygous mice did not exhibit an increased susceptibility to arrhythmia upon catecholamine challenge in vivo, and there were no premature deaths up to 1 yr of age. These findings suggest that a partial downregulation of junctin enhances sarcoplasmic reticulum Ca(2+) cycling but does not elicit cardiac arrhythmias even in the context of increased Na(+)-Ca(2+) exchanger activity.
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Extracellular ATP signaling is mediated by H?O? and cytosolic Ca²? in the salt response of Populus euphratica cells.
PLoS ONE
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Extracellular ATP (eATP) has been implicated in mediating plant growth and antioxidant defense; however, it is largely unknown whether eATP might mediate salinity tolerance. We used confocal microscopy, a non-invasive vibrating ion-selective microelectrode, and quantitative real time PCR analysis to evaluate the physiological significance of eATP in the salt resistance of cell cultures derived from a salt-tolerant woody species, Populus euphratica. Application of NaCl (200 mM) shock induced a transient elevation in [eATP]. We investigated the effects of eATP by blocking P2 receptors with suramin and PPADS and applying an ATP trap system of hexokinase-glucose. We found that eATP regulated a wide range of cellular processes required for salt adaptation, including vacuolar Na? compartmentation, Na?/H? exchange across the plasma membrane (PM), K? homeostasis, reactive oxygen species regulation, and salt-responsive expression of genes related to Na?/H? homeostasis and PM repair. Furthermore, we found that the eATP signaling was mediated by H?O? and cytosolic Ca²? released in response to high salt in P. euphratica cells. We concluded that salt-induced eATP was sensed by purinoceptors in the PM, and this led to the induction of downstream signals, like H?O? and cytosolic Ca²?, which are required for the up-regulation of genes linked to Na?/H? homeostasis and PM repair. Consequently, the viability of P. euphratica cells was maintained during a prolonged period of salt stress.
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Novel role of HAX-1 in ischemic injury protection involvement of heat shock protein 90.
Circ. Res.
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Ischemic heart disease is characterized by contractile dysfunction and increased cardiomyocyte death, induced by necrosis and apoptosis. Increased cell survival after an ischemic insult is critical and depends on several cellular pathways, which have not been fully elucidated.
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Genome-wide association study in Han Chinese identifies four new susceptibility loci for coronary artery disease.
Nat. Genet.
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We performed a meta-analysis of 2 genome-wide association studies of coronary artery disease comprising 1,515 cases and 5,019 controls followed by replication studies in 15,460 cases and 11,472 controls, all of Chinese Han ancestry. We identify four new loci for coronary artery disease that reached the threshold of genome-wide significance (P < 5 × 10(-8)). These loci mapped in or near TTC32-WDR35, GUCY1A3, C6orf10-BTNL2 and ATP2B1. We also replicated four loci previously identified in European populations (in or near PHACTR1, TCF21, CDKN2A-CDKN2B and C12orf51). These findings provide new insights into pathways contributing to the susceptibility for coronary artery disease in the Chinese Han population.
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Ablation of junctin or triadin is associated with increased cardiac injury following ischaemia/reperfusion.
Cardiovasc. Res.
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Junctin and triadin are calsequestrin-binding proteins that regulate sarcoplasmic reticulum (SR) Ca(2+) release by interacting with the ryanodine receptor. The levels of these proteins are significantly down-regulated in failing human hearts. However, the significance of such decreases is currently unknown. Here, we addressed the functional role of these accessory proteins in the hearts responses to ischaemia/reperfusion (I/R) injury.
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JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.