Air Power in Low-Intensity Conflict

1987 ◽  
Author(s):  
Gary N. Schneider
Keyword(s):  
Air Power ◽  
Low Intensity

Rolling Thunder and Linebacker Campaigns: The North Vietnamese View

2001 ◽  
Vol 10 (3-4) ◽  
pp. 197-230
Author(s):  
Merle L. Pribbenow
Keyword(s):  
World War Ii ◽  
World War ◽  
Combat Experience ◽  
Air Power ◽  
Desert Storm ◽  
Low Intensity ◽  
The North ◽  
The World ◽  
North Vietnam ◽  
Iraqi Freedom

AbstractNorth Vietnam has the dubious distinction of having more combat experience against U.S. air power than any other nation in the world. Rolling Thunder, the first U.S. bombing campaign against North Vietnam (1965–68), lasted longer than U.S. air operations in Europe during World War II. When one adds the 1972 Linebacker air campaign against North Vietnam and the almost nine-year bombing campaign against the Ho Chi Minh Trail in Laos, only Iraq, with the air campaigns of Operations Desert Storm and Iraqi Freedom book-ending a twelve-year (1991–2003), low-intensity confrontation against U.S. aircraft over the no fly zones, faced U.S. air attacks longer. The air battles over Iraq, however, cannot be compared with the battles fought in the skies over North Vietnam. During the course of the war, more than 1,100 U.S. fixed wing aircraft were lost in combat operations.

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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