The Experts below are selected from a list of 210 Experts worldwide ranked by ideXlab platform
Jos F M Smits - One of the best experts on this subject based on the ideXlab platform.
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the infarcted myocardium simply Dead Tissue or a lively target for therapeutic interventions
Cardiovascular Research, 1999Co-Authors: J P M Cleutjens, W M Blankesteijn, Mat J A P Daemen, Jos F M SmitsAbstract:Time for primary review 32 days. It has been known for many years that infarction of the heart induces prominent alterations of cardiac structure. The most apparent is the scarring of the infarct. Structural changes after infarction are, however, not limited to the infarcted area, but also extend into the non-infarcted myocardium. Changes in the non-infarcted myocardium include hypertrophy of the cardiomyocytes, growth of the capillary network, and an increase in interstitial collagen. Cardiac structure is a major determinant of function, which is depressed after myocardial infarction (MI). After infarction, both short term and long term compensatory or regulatory mechanisms are activated. Often these mechanisms also affect cardiac structure. Although activation of these compensatory mechanisms may be beneficial early after infarction, they may have adverse effects, when activation is continued for a longer time. Indeed, pharmacological treatments that block the long term activation of these compensatory mechanisms, like angiotensin converting enzyme inhibitors (ACEI) that block the renin—angiotensin system (RAS), have been shown to improve cardiac function after infarction. Although we know that cardiac function and structure are closely related and do indeed both change after infarction, it is largely unknown what the exact structural component is that causes the reduction in cardiac function after infarction. Also it is not clear which structural component should be targeted for effective pharmacotherapy after infarction. In this review we attempt to clarify the structural alterations after infarction. We and others have focused for many years on the potential importance of changes in the vital non-infarcted myocardium and, indeed, found several alterations in cardiac structure after infarction and effects thereon of drugs that improved cardiac function. However, recent data in animal studies and humans point to the importance of the infarct itself as a potential target for intervention. The infarct appears to be more than … * Corresponding author. Tel.: +31-43-387-6631; fax: +31-43-387-6613 jcl{at}lpat.azm.nl
J P M Cleutjens - One of the best experts on this subject based on the ideXlab platform.
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the infarcted myocardium simply Dead Tissue or a lively target for therapeutic interventions
Cardiovascular Research, 1999Co-Authors: J P M Cleutjens, W M Blankesteijn, Mat J A P Daemen, Jos F M SmitsAbstract:Time for primary review 32 days. It has been known for many years that infarction of the heart induces prominent alterations of cardiac structure. The most apparent is the scarring of the infarct. Structural changes after infarction are, however, not limited to the infarcted area, but also extend into the non-infarcted myocardium. Changes in the non-infarcted myocardium include hypertrophy of the cardiomyocytes, growth of the capillary network, and an increase in interstitial collagen. Cardiac structure is a major determinant of function, which is depressed after myocardial infarction (MI). After infarction, both short term and long term compensatory or regulatory mechanisms are activated. Often these mechanisms also affect cardiac structure. Although activation of these compensatory mechanisms may be beneficial early after infarction, they may have adverse effects, when activation is continued for a longer time. Indeed, pharmacological treatments that block the long term activation of these compensatory mechanisms, like angiotensin converting enzyme inhibitors (ACEI) that block the renin—angiotensin system (RAS), have been shown to improve cardiac function after infarction. Although we know that cardiac function and structure are closely related and do indeed both change after infarction, it is largely unknown what the exact structural component is that causes the reduction in cardiac function after infarction. Also it is not clear which structural component should be targeted for effective pharmacotherapy after infarction. In this review we attempt to clarify the structural alterations after infarction. We and others have focused for many years on the potential importance of changes in the vital non-infarcted myocardium and, indeed, found several alterations in cardiac structure after infarction and effects thereon of drugs that improved cardiac function. However, recent data in animal studies and humans point to the importance of the infarct itself as a potential target for intervention. The infarct appears to be more than … * Corresponding author. Tel.: +31-43-387-6631; fax: +31-43-387-6613 jcl{at}lpat.azm.nl
Ramkumar Menon - One of the best experts on this subject based on the ideXlab platform.
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human fetal membranes at term Dead Tissue or signalers of parturition
Placenta, 2016Co-Authors: Ramkumar MenonAbstract:Various endocrine, immune, and mechanical factors produced by feto-maternal compartments at term increase intrauterine inflammatory loads to induce labor. The role of fetal (placental) membranes (amniochorion) as providers of parturition signals has not been well investigated. Fetal membranes line the intrauterine cavity and grow with and protect the fetus. Fetal membranes exist as an entity between the mother and fetus and perform unique functions during pregnancy. Membranes undergo a telomere-dependent p38 MAPK-induced senescence and demonstrate a decline in functional and mechanical abilities at term, showing signs of aging. Fetal membrane senescence is also allied with completion of fetal maturation at term as the fetus readies for delivery, which may also indicate the end of independent life and longevity of fetal membranes as their functional role concludes. Fetal membrane senescence is accelerated at term because of oxidative stress and increased stretching. Senescent fetal membranes cells produce senescence-associated secretory phenotype (SASP-inflammation) and also release proinflammatory damage-associated molecular patterns (DAMPs), namely HMGB1 and cell-free fetal telomere fragments. In a feedback loop, SASP and DAMPs increase senescence and enhance the inflammatory load to promote labor. Membranes increase the inflammatory load to disrupt homeostatic balance to transition quiescent uterine Tissues toward a labor phenotype. Therefore, along with other well-described labor-promoting signals, senescent fetal membranes may also contribute to human term parturition.
Jenise M Snyder - One of the best experts on this subject based on the ideXlab platform.
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macrophyte root and rhizome decay the impact of nutrient enrichment and the use of live versus Dead Tissue in decomposition studies
Biogeochemistry, 2015Co-Authors: Jenise M Snyder, Eliska RejmankovaAbstract:The decomposition of roots and rhizomes of two macrophytes, Eleocharis cellulosa and Typha domingensis, was studied in oligotrophic phosphorus (P) limited marshes of northern Belize. The experiment was conducted in long-term control and P enriched plots in five limestone-based inland marshes. Decomposition of naturally senescent root and rhizome litter was studied over 9 months using litterbags. Belowground litter was acquired by growing plants in unenriched (control) or P enriched marsh soils for 5 months. Plants were then allowed to naturally senesce using a split root design, which promoted nutrient retranslocation. The resulting senescent litter had 30 % higher C:P and 40 % lower P content than living roots and rhizomes. There were no differences in C:N among treatments or senescent versus live litter. Litterbags, filled with control or enriched root and rhizome litter, were buried in the upper 10–14 cm soil in the corresponding plot of each marsh. Differences in the rate of decay between species were greatest for rhizome Tissue, with Typha decaying more than twice as fast as Eleocharis. For both species, however, Tissue P enrichment had no effect on coarse root and rhizome decay. Enhanced root production from P enrichment, coupled with no change in decay, should lead to enhanced accretion over time. Additional tests, using litterbags filled with living roots and rhizomes, yielded dramatically different results between treatments compared to senescent Tissue. Results from senescent belowground Tissue also differed from shoot decomposition. Caution should be exercised when inferring belowground decomposition from live Tissue and aboveground rates of decay.
Melvin T Tyree - One of the best experts on this subject based on the ideXlab platform.
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experimental evidence for negative turgor pressure in small leaf cells of robinia pseudoacacia l versus large cells of metasequoia glyptostroboides hu et w c cheng 1 evidence from pressure volume curve analysis of Dead Tissue
Plant Cell and Environment, 2017Co-Authors: Dongmei Yang, Yiting Ding, Melvin T TyreeAbstract:This paper provides a mini-review of evidence for negative turgor pressure in leaf cells starting with experimental evidence in the late 1950s and ending with biomechanical models published in 2014. In the present study, biomechanical models were used to predict how negative turgor pressure might be manifested in Dead Tissue, and experiments were conducted to test the predictions. The main findings were as follows: (i) Tissues killed by heating to 60 or 80 °C or by freezing in liquid nitrogen all became equally leaky to cell sap solutes and all seemed to pass freely through the cell walls. (ii) Once cell sap solutes could freely pass the cell walls, the shape of pressure-volume curves was dramatically altered between living and Dead cells. (iii) Pressure-volume curves of Dead Tissue seem to measure negative turgor defined as negative when inside minus outside pressure is negative. (iv) Robinia pseudoacacia leaves with small palisade cells had more negative turgor than Metasequoia glyptostroboides with large cells. (v) The absolute difference in negative turgor between R. pseudoacacia and M. glyptostroboides approached as much as 1.0 MPa in some cases. The differences in the manifestation of negative turgor in living versus Dead Tissue are discussed.