Steady-state assemblages in a Mediterranean hypertrophic reservoir. The role of Microcystis ecomorphological variability in maintaining an apparent equilibrium

Hydrobiologia ◽  
2003 ◽  
Vol 502 (1-3) ◽  
pp. 133-143 ◽  
Author(s):  
Luigi Naselli-Flores ◽  
Rossella Barone
Keyword(s):  
Steady State ◽  
Apparent Equilibrium ◽  
Hypertrophic Reservoir ◽  
Steady State Assemblages

scholarly journals The critical role of T cells in glucocorticoid-induced osteoporosis

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Lin Song ◽  
Lijuan Cao ◽  
Rui Liu ◽  
Hui Ma ◽  
Yanan Li ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
Steady State ◽  
Side Effects ◽  
Critical Role ◽  
Wild Type ◽  
Receptor Activator ◽  
Steady State Levels ◽  
Induced Apoptosis

AbstractGlucocorticoids (GC) are widely used clinically, despite the presence of significant side effects, including glucocorticoid-induced osteoporosis (GIOP). While GC are believed to act directly on osteoblasts and osteoclasts to promote osteoporosis, the detailed underlying molecular mechanism of GC-induced osteoporosis is still not fully elucidated. Here, we show that lymphocytes play a pivotal role in regulating GC-induced osteoporosis. We show that GIOP could not be induced in SCID mice that lack T cells, but it could be re-established by adoptive transfer of splenic T cells from wild-type mice. As expected, T cells in the periphery are greatly reduced by GC; instead, they accumulate in the bone marrow where they are protected from GC-induced apoptosis. These bone marrow T cells in GC-treated mice express high steady-state levels of NF-κB receptor activator ligand (RANKL), which promotes the formation and maturation of osteoclasts and induces osteoporosis. Taken together, these findings reveal a critical role for T cells in GIOP.

scholarly journals The role of noise on the steady state distributions of phytoplankton populations

2016 ◽  
Vol 2016 (5) ◽  
pp. 054044 ◽  
Author(s):  
D Valenti ◽  
G Denaro ◽  
F Conversano ◽  
C Brunet ◽  
A Bonanno ◽  
...  
Keyword(s):  
Steady State

scholarly journals Accumulation of Prostacyclin in Rat Brain during Haemorrhagic Hypotension—Possible Role of PGI2 in Autoregulation

1984 ◽  
Vol 4 (1) ◽  
pp. 107-109 ◽  
Author(s):  
E. Shohami ◽  
A. Sidi
Keyword(s):  
Blood Pressure ◽  
Steady State ◽  
Control Group ◽  
Prostaglandin E ◽  
Cortical Tissue ◽  
Arterial Blood ◽  
Haemorrhagic Hypotension ◽  
Potent Vasodilator ◽  
Prostaglandin F

The effect of haemorrhagic hypotension on the levels of prostaglandin E2 (PGE2), thromboxane B2 (TXB2), and 6-keto prostaglandin F1α (6-keto-PGF1α) in cortical tissue of rats was studied. Lightly anesthetized rats were subjected to steady-state hypotension for 15 min, with a mean arterial blood pressure of 80, 60, and 40 mm Hg, and compared to a control group of normotensive rats. No significant change was found in the levels of PGE2 and TXB2. The level of 6-keto-PGF1α increased from 7.8 ± 0.9 to 14.1 ± 1.9 pg/mg protein (p < 0.02) at 80 mm Hg. Our findings suggest that prostacyclin, which is a potent vasodilator, might play a role in setting the lower limit of the autoregulation range.

scholarly journals Role of Ca2+ in pyruvate dehydrogenase interconversion in brain mitochondria and synaptosomes

1985 ◽  
Vol 227 (1) ◽  
pp. 129-136 ◽  
Author(s):  
R G Hansford ◽  
F Castro
Keyword(s):  
Plasma Membrane ◽  
Steady State ◽  
Pyruvate Dehydrogenase ◽  
Maximal Activity ◽  
Brain Mitochondria ◽  
Ruthenium Red ◽  
Ion Concentration ◽  
Maximal Effect ◽  
State Content

The steady-state content of active (dephospho) pyruvate dehydrogenase (PDHA) of suspensions of coupled rat brain mitochondria oxidizing succinate was found to be markedly increased with increasing free Ca2+ ion concentration of the medium, with a half-maximal effect at 10(-6.43) M Ca2+. Other ions were present in these studies at concentrations appropriate for the cytosol. Depolarization of the plasma membrane of synaptosomes caused an increase in the steady-state content of PDHA, with veratridine giving a larger increase than depolarization by 33 mM-KCl. Values were 68 +/- 1% (n = 13) and 81 +/- 1% (n = 19) of maximal activity, for control incubations and incubations in the presence of 30 microM-veratridine, respectively. Measurements of cytosolic free Ca2+ concentrations ([Ca2+]cyt.) in these suspensions of synaptosomes, with the use of the fluorescent Ca2+-indicator Quin-2, indicated an increase on depolarization, with the change due to 30 microM-veratridine being larger in extent than that due to 33 mM-KCl. Values were 217 +/- 21 nM (n = 15), 544 +/- 48 nM (n = 15) and 783 +/- 75 nM (n = 14) for control, KCl-depolarized and veratridine-depolarized synaptosomes respectively. Experiments in which synaptosomes were treated with Ruthenium Red, an inhibitor of mitochondrial Ca2+ uptake, gave much lower resting contents of PDHA (42 +/- 2% of maximal), but failed to prevent totally an increase on depolarization. Addition of an excess of EGTA to the synaptosomal suspension just before the addition of veratridine resulted in a partial diminution in the response of PDHA content. Parallel studies with Quin-2 indicated no increase in [Ca2+]cyt. on addition of veratridine, under these conditions. Thus an increase in [Ca2+]cyt. forms only a part of the mechanism whereby pyruvate dehydrogenase interconversion responds to depolarization. A decrease in the ATP/ADP ratio may also be important, as inferred from the results of experiments with ouabain, which inhibits the Na+ + K+-dependent ATPase.

The role of surface topography and normal load in the initiation of ratchetting-peak friction, seizure, scuffing, and elastic shakedown

2021 ◽  
pp. 1-12
Author(s):  
Vimal Edachery ◽  
V. Swamybabu ◽  
Gurupatham Anand ◽  
Paramasamy Manikandan ◽  
Satish V. Kailas
Keyword(s):  
Steady State ◽  
Surface Topography ◽  
Sliding Wear ◽  
Friction And Wear ◽  
Critical Parameter ◽  
Normal Load ◽  
Sliding Direction ◽  
Elastic Shakedown ◽  
Lubrication Conditions

Abstract Surface topography is a critical parameter that can influence friction and wear in engineering applications. In this work, the influence of surface topography directionality on seizure and scuffing initiation during tribological interactions is explored. For this, unidirectional sliding wear experiments were carried out in immersed lubrication conditions for various normal loads. The tribological interactions were studied using EN31-60 HRC flats and SAE52100-60HRC pins in a sphere on flat configuration. The results show that, in some cases, the sliding interactions in the initial cycles lead to a high friction coefficient of up to ∼0.68 in lubricated conditions, which was termed as ‘peak friction’, and this was accompanied by scuffing. The existence of peak friction was found to be dependent on surface topography directionality, especially when the directionality in topography was parallel to the sliding direction. Continuous ratchetting was found to be the cause of peak friction which was accompanied by seizure and scuffing. When the topography directionality was perpendicular or independent of sliding direction, elastic shakedown occurred at earlier cycles and prevented peak friction initiation, scuffing and also facilitated for higher steady-state friction values.

scholarly journals Role of Oxidative Stress in Heart Failure: Insights from Gene Transfer Studies

Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1645
Author(s):  
Bart De Geest ◽  
Mudit Mishra
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Gene Therapy ◽  
Steady State ◽  
Gene Transfer ◽  
Oxidative Modification ◽  
Heme Oxygenase 1 ◽  
Therapy Studies ◽  
Pathological Remodeling

Under physiological circumstances, there is an exquisite balance between reactive oxygen species (ROS) production and ROS degradation, resulting in low steady-state ROS levels. ROS participate in normal cellular function and in cellular homeostasis. Oxidative stress is the state of a transient or a persistent increase of steady-state ROS levels leading to disturbed signaling pathways and oxidative modification of cellular constituents. It is a key pathophysiological player in pathological hypertrophy, pathological remodeling, and the development and progression of heart failure. The heart is the metabolically most active organ and is characterized by the highest content of mitochondria of any tissue. Mitochondria are the main source of ROS in the myocardium. The causal role of oxidative stress in heart failure is highlighted by gene transfer studies of three primary antioxidant enzymes, thioredoxin, and heme oxygenase-1, and is further supported by gene therapy studies directed at correcting oxidative stress linked to metabolic risk factors. Moreover, gene transfer studies have demonstrated that redox-sensitive microRNAs constitute potential therapeutic targets for the treatment of heart failure. In conclusion, gene therapy studies have provided strong corroborative evidence for a key role of oxidative stress in pathological remodeling and in the development of heart failure.

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