Olga Georges Picot Un Official Fan Site Tribute

Olga Georges Picot : This Is An Un Official Fan Site Tribute
Olga Georges Picot
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Olga Georges-Picot (6 January 1940 – 19 June 1997) was a French actress. She was a great-niece of François Georges-Picot.[1] Contents 1 Early life 2 Career 3 Filmography 4 References 5 External links Early life Born in Shanghai, in Japanese-occupied China, she was the daughter of Guillaume Georges-Picot, the French Ambassador to China, and a Russian mother, Anastasia Vyacheslavovna Mironovich. She attended the International School in Geneva in the early fifties with her sister. She also attended the Lycée français de New York (Class of 1958).[2] She studied acting at the Actors Studio in Paris.
Career Her acting career included roles in French and English films, and on television. She was featured in Playboy Magazine’s "Sex in Cinema" column, and also on the front cover of the periodical Adam. She appeared in three mainstream films: Denise, the OAS mole, in The Day of the Jackal (1973); Countess Alexandrovna in Woody Allen’s Love and Death (1975); and Julie Anderson in Basil Dearden’s The Man Who Haunted Himself (1970). Her break-through role in the movies was as Catrine in the Alain Resnais’s film Je t'aime, je t'aime (1968). Earlier that year, she had appeared in the French television movie Thibaud the Crusader (1968). Filmography Year Title Role Notes 1962 Tales of Paris La secrétaire (segment "Ella") 1967 Two for the Road Joanna's Touring Friend Uncredited 1968 Je t'aime, je t'aime Catrine 1968 Farewell, Friend Isabelle Moreau

1968 The Other People Elsa 1968 Summit 1969 Catherine, il suffit d'un amour [fr] Catherine 1970 The Man Who Haunted Himself Julie Anderson 1970 Connecting Rooms Claudia 1971 La cavale Nadine 1972 The Man Who Quit Smoking Gunhild 1973 La révélation Clarie 1973 Un Homme libre Nicole Lefèvre 1973 The Day of the Jackal Denise 1973 Le feu aux lèvres Christine Benoît 1973 Les Confidences érotiques d'un lit trop accueillant Dominique 1973 Féminin-féminin Marie-Hélène 1974 Successive slidings of pleasure Nora / lawyer 1974 Persecution Monique Kalfon aka Sheba, The Graveyard, The Terror of Sheba 1974 Härte 10 [de] Nadine Mercier TV Mini-Series, 6 episodes 1975 Children of Rage Leylah Saleh 1975 Love and Death Countess Alexandrovna 1977 Goodbye Emmanuelle Florence 1978 Brigade mondaine 1984 Rebelote Suzanne Chauveau, la mère A thrombus, colloquially called a blood clot, is the final product of the blood coagulation step in hemostasis. There are two components to a thrombus: aggregated platelets and red blood cells that form a plug, and a mesh of cross-linked fibrin protein. The substance making up a thrombus is sometimes called cruor. A thrombus is a healthy response to injury intended to prevent bleeding, but can be harmful in thrombosis, when clots obstruct blood flow through healthy blood vessels. Mural thrombi are thrombi that adhere to the wall of a blood vessel. They occur in large vessels such as the heart and aorta, and can restrict blood flow but usually do not block it entirely. They appear grey-red with alternating light and dark lines (known as lines of Zahn) which represent bands of entrapped white blood cells and red blood cells (darker). Contents 1 Cause 2 Classification 3 Pathophysiology 3.1 Formation 4 Prevention and treatment 5 Prognosis 6 See also 7 References 8 External links Cause Virchow's triad describes the pathogenesis of thrombus formation:[1][2] Endothelial injury: Injury to the endothelium (interior surface of blood vessel), causing platelet activation and aggregation Common causes include: trauma, smoking, hypertension, atheroma Stasis: Blood stasis promotes greater contact between platelets/coagulative factors with vascular endothelium. Common causes of stasis include anything that leads to prolonged immobility and reduced blood flow such as: trauma/broken bones and extended air travel Hypercoagulability (also called thrombophilia; any disorder of the blood that predisposes to thrombosis) Common causes include: cancer (leukaemia), Factor V mutation (Leiden) - prevents Factor V inactivation leading to increased coagulability. Disseminated intravascular coagulation (DIC) involves widespread microthrombi formation throughout the majority of the blood vessels. This is due to excessive consumption of coagulation factors and subsequent activation of fibrinolysis using all of the body's available platelets and clotting factors. The end result is hemorrhaging and ischaemic necrosis of tissue/organs. Causes are septicaemia, acute leukaemia, shock, snake bites, fat emboli from broken bones, or other severe traumas. DIC may also be seen in pregnant females. Treatment involves the use of fresh frozen plasma to restore the level of clotting factors in the blood, as well as platelets and heparin to prevent further thrombi formation. Classification Thrombi are classified into two major groups depending on their location and the relative amount of platelets and red blood cells (RBCs).[3] The two major groups are: Arterial or white thrombi (characterized by predominance of platelets) Venous or red thrombi (characterized by predominance of red blood cells). Pathophysiology Animation of the formation of an occlusive thrombus in a vein. A few platelets attach themselves to the valve lips, constricting the opening and causing more platelets and red blood cells to aggregate and coagulate. Coagulation of unmoving blood on both sides of the blockage may propagate a clot in both directions. A thrombus occurs when the hemostatic process, which normally occurs in response to injury, becomes activated in an uninjured or slightly injured vessel. A thrombus in a large blood vessel will decrease blood flow through that vessel (termed a mural thrombus). In a small blood vessel, blood flow may be completely cut off (termed an occlusive thrombus), resulting in death of tissue supplied by that vessel. If a thrombus dislodges and becomes free-floating, it is considered an embolus. Some of the conditions which increase the risk of blood clots developing include atrial fibrillation (a form of cardiac arrhythmia), heart valve replacement, a recent heart attack (also known as a myocardial infarction), extended periods of inactivity (see deep venous thrombosis), and genetic or disease-related deficiencies in the blood's clotting abilities. Formation Platelet activation occurs through injuries that damage the endothelium of the blood vessels, exposing the enzyme called factor VII, a protein normally circulating within the vessels, to the tissue factor, which is a protein encoded by the F3 gene. The platelet activation can potentially cause a cascade, eventually leading to the formation of the thrombus.[4] This process is regulated

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