Changes induced on the prolamellar body of pea seedlings by white, red and blue low intensity light

PROTOPLASMA ◽  
1986 ◽  
Vol 131 (2) ◽  
pp. 166-173 ◽  
Author(s):  
A. Mostowska
Keyword(s):  
Prolamellar Body ◽  
Low Intensity ◽  
Pea Seedlings

scholarly journals Stereometrical analysis of number and size of prolamellar bodies during pea chloroplast development

2014 ◽  
Vol 54 (1) ◽  
pp. 53-63 ◽  
Author(s):  
Agnieszka Mostowska
Keyword(s):  
Chloroplast Development ◽  
Prolamellar Body ◽  
Direct Information ◽  
Low Intensity ◽  
Prolamellar Bodies ◽  
Pea Seedlings ◽  
Gradual Transformation

The plastid prolamelar bodies in dark-grown pea seedlings undergo gradual transformation and decay after illumination with low intensity light. Random micrographs do not give direct information concerning the sizes and average numbers of prolamellar bodies in a plastid. These values were obtained after evaluation by a stereometrical method from the ratio of polamellar bodies sizes to the plastid size and from the frequency of prolamellar body sections of a given diameter. Plastids of dark-grown seedlings contained on the average at least one prolamellar body. After illumination the size of the bodies decreased rapidly owing to dispersion into primary thylakoids and split into much smaller numerous prolamellar bodies.

Low-Intensity Cognitive Behavioral Therapy

2017 ◽  
Vol 2 (1) ◽  
pp. 31-36
Author(s):  
Pascal Wabnitz ◽  
Michael Schulz ◽  
Michael Löhr ◽  
André Nienaber
Keyword(s):  
Cognitive Behavioral Therapy ◽  
Behavioral Therapy ◽  
Cognitive Behavioral ◽  
Low Intensity

Maori adaptation of a low intensity mental health intervention in primary care

2012 ◽  
Author(s):  
Fiona Mathieson ◽  
Kara Mihaere ◽  
Sunny Collings ◽  
Anthony Dowell ◽  
James Stanley
Keyword(s):  
Mental Health ◽  
Primary Care ◽  
Health Intervention ◽  
Mental Health Intervention ◽  
Low Intensity

Inhibition rather than Enhancement of Hemostatic System Activation during Initiation of Oral Anticoagulant Treatment

1997 ◽  
Vol 77 (04) ◽  
pp. 685-689 ◽  
Author(s):  
Paul A Kyrle ◽  
Johannes Brockmeier ◽  
Ansgar Weltermann ◽  
Sabine Eichinger ◽  
Wolfgang Speiser ◽  
...  
Keyword(s):  
High Intensity ◽  
Oral Anticoagulant ◽  
Protein C ◽  
Venous Blood ◽  
Rapid Decline ◽  
Oral Anticoagulant Treatment ◽  
Shed Blood ◽  
Low Intensity ◽  
Hemostatic System ◽  
System Activation

SummaryCoumarin-induced skin necrosis is believed to be due to a transient hypercoagulable state resulting from a more rapid decline of the protein C activity relative to that of coagulation factors (F) II, IX and X during initiation of oral anticoagulant therapy. We studied hemostatic system activation during early oral anticoagulant treatment with a technique that investigates coagulation activation in the microcirculation.We determined in 10 healthy volunteers the concentrations of prothrombin fragment F1+2 (f1.2) and thrombin-antithrombin complex (TAT) in blood emerging from an injury of the microvasculature (bleeding time incision) before and after initiation of both high-inten- sity and low-intensity coumarin therapy. In addition, f1.2, TAT, activated F VII (F Vila) and the activities of FII, F VII, F X and protein C were measured in venous blood.A rapid decline of F VII and protein C was observed in venous blood with activities at 24 h of 7 ± 1% and 43 ± 2%, respectively, during the high-intensity regimen. A 20 to 30% reduction of f1.2 and TAT was seen in venous blood at 72 h with no major difference between the high- and the low-intensity regimen. F Vila levels were substantially affected by anticoagulation with a >90% reduction at 48 h during the high-intensity regimen. Following high-intensity coumarin, a >50% decrease in the fl.2 and TAT levels was found in shed blood at 48 h suggesting substantial inhibition of thrombin generation during early oral anticoagulation. An increase in the f1.2 and TAT levels was seen neither in shed blood nor in venous blood.Our data do not support the concept of a transient imbalance between generation and inhibition of thrombin as the underlying pathomechanism of coumarin-induced skin nekrosis.

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