This document discusses blood types and blood coagulation. It covers the main blood types (A, B, AB, and O) determined by the presence or absence of antigens, and the Rh factor. It describes how improper blood matching can lead to agglutination and hemolysis during transfusion. The coagulation process is summarized, from platelet plug formation to the coagulation cascade and production of thrombin and fibrin. Common coagulation factors are identified. Causes of bleeding disorders like hemophilia and thrombocytopenia are outlined.
This document provides an overview of the coagulation system. It begins with an introduction to the coagulation cascade and hemostasis. It then discusses the intrinsic and extrinsic pathways in more detail, focusing on the complexes formed and the factors involved such as tissue factor and thrombin. The document also covers anticoagulation processes mediated by the endothelium like heparan sulfate and protein C. It concludes with explanations of fibrinolysis and the role of vitamin K in carboxylating coagulation factors.
The document lists 11 coagulation factors involved in the blood clotting process, along with their names, sources, and in some cases additional details. Factor III is produced by damaged tissues and activated platelets. Factors I, II, V, VII, VIII, IX, X, XI, and XIII are produced by the liver, while factors IV, V, and XIII also have additional sources.
The cascade theory describes blood coagulation as a series of biochemical reactions that converts soluble fibrinogen into insoluble fibrin clot. It involves the intrinsic and extrinsic pathways that activate coagulation factors in a cascade-like manner, culminating in a common pathway where thrombin converts fibrinogen to fibrin. Feedback mechanisms tightly regulate clot formation to prevent excessive coagulation.
Platelets play a key role in hemostasis and thrombosis. They become activated when endothelial cells are damaged, adhering to exposed collagen and releasing substances like ADP and thromboxane A2 that amplify recruitment and activation of additional platelets. Activated platelets undergo conformational changes and secrete procoagulant factors from granules, promoting fibrin formation and stabilization of thrombi. Strong agonists like thrombin and collagen induce intracellular signaling leading to aggregation, while weaker agonists like ADP stimulate secondary pathways. Platelets also release inflammatory mediators that can promote endothelial dysfunction. Antiplatelet drugs inhibit pathways of platelet activation to reduce thrombosis.
Secondary Haemostasis involves the formation of fibrin clots via the blood coagulation cascade. This involves complex sequential reactions between coagulation factors. The coagulation factors are classified based on their physical properties like molecular weight or functional properties like being substrates, cofactors, or enzymes. Vitamin K plays an important role by allowing coagulation factors to bind to phospholipid surfaces. The coagulation cascade is tightly regulated by naturally occurring inhibitors like antithrombin III and protein C to prevent excessive clotting.
Secondary hemostasis - coagulation cascades and lab testsharveenbhusari
This document provides an overview of coagulation factors and mechanisms involved in secondary hemostasis. It describes the intrinsic and extrinsic pathways, key coagulation factors such as fibrinogen, prothrombin, thromboplastin, and von Willebrand factor. It also discusses the fibrinolytic system, natural inhibitors of coagulation, and common laboratory tests used to evaluate coagulation, including specimen collection methods.
The coagulation system involves a cascade of enzymatic reactions that ultimately result in fibrin clot formation. The cascade can be initiated through either the intrinsic or extrinsic pathway, both of which involve a series of coagulation factor zymogens being activated into active enzyme forms. This leads to thrombin generation and conversion of fibrinogen into fibrin. A number of processes also act to regulate coagulation and prevent excessive clotting, including antithrombin III, protein C, and fibrinolysis.
This document discusses blood types and blood coagulation. It covers the main blood types (A, B, AB, and O) determined by the presence or absence of antigens, and the Rh factor. It describes how improper blood matching can lead to agglutination and hemolysis during transfusion. The coagulation process is summarized, from platelet plug formation to the coagulation cascade and production of thrombin and fibrin. Common coagulation factors are identified. Causes of bleeding disorders like hemophilia and thrombocytopenia are outlined.
This document provides an overview of the coagulation system. It begins with an introduction to the coagulation cascade and hemostasis. It then discusses the intrinsic and extrinsic pathways in more detail, focusing on the complexes formed and the factors involved such as tissue factor and thrombin. The document also covers anticoagulation processes mediated by the endothelium like heparan sulfate and protein C. It concludes with explanations of fibrinolysis and the role of vitamin K in carboxylating coagulation factors.
The document lists 11 coagulation factors involved in the blood clotting process, along with their names, sources, and in some cases additional details. Factor III is produced by damaged tissues and activated platelets. Factors I, II, V, VII, VIII, IX, X, XI, and XIII are produced by the liver, while factors IV, V, and XIII also have additional sources.
The cascade theory describes blood coagulation as a series of biochemical reactions that converts soluble fibrinogen into insoluble fibrin clot. It involves the intrinsic and extrinsic pathways that activate coagulation factors in a cascade-like manner, culminating in a common pathway where thrombin converts fibrinogen to fibrin. Feedback mechanisms tightly regulate clot formation to prevent excessive coagulation.
Platelets play a key role in hemostasis and thrombosis. They become activated when endothelial cells are damaged, adhering to exposed collagen and releasing substances like ADP and thromboxane A2 that amplify recruitment and activation of additional platelets. Activated platelets undergo conformational changes and secrete procoagulant factors from granules, promoting fibrin formation and stabilization of thrombi. Strong agonists like thrombin and collagen induce intracellular signaling leading to aggregation, while weaker agonists like ADP stimulate secondary pathways. Platelets also release inflammatory mediators that can promote endothelial dysfunction. Antiplatelet drugs inhibit pathways of platelet activation to reduce thrombosis.
Secondary Haemostasis involves the formation of fibrin clots via the blood coagulation cascade. This involves complex sequential reactions between coagulation factors. The coagulation factors are classified based on their physical properties like molecular weight or functional properties like being substrates, cofactors, or enzymes. Vitamin K plays an important role by allowing coagulation factors to bind to phospholipid surfaces. The coagulation cascade is tightly regulated by naturally occurring inhibitors like antithrombin III and protein C to prevent excessive clotting.
Secondary hemostasis - coagulation cascades and lab testsharveenbhusari
This document provides an overview of coagulation factors and mechanisms involved in secondary hemostasis. It describes the intrinsic and extrinsic pathways, key coagulation factors such as fibrinogen, prothrombin, thromboplastin, and von Willebrand factor. It also discusses the fibrinolytic system, natural inhibitors of coagulation, and common laboratory tests used to evaluate coagulation, including specimen collection methods.
The coagulation system involves a cascade of enzymatic reactions that ultimately result in fibrin clot formation. The cascade can be initiated through either the intrinsic or extrinsic pathway, both of which involve a series of coagulation factor zymogens being activated into active enzyme forms. This leads to thrombin generation and conversion of fibrinogen into fibrin. A number of processes also act to regulate coagulation and prevent excessive clotting, including antithrombin III, protein C, and fibrinolysis.
Coagulation: In medicine, the clotting of blood. The process by which the blood clots to form solid masses, or clots.
More than 30 types of cells and substances in blood affect clotting. The process is initiated by blood platelets. Platelets produce a substance that combines with calcium ions in the blood to form thromboplastin, which in turn converts the protein prothrombin into thrombin in a complex series of reactions. Thrombin, a proteolytic enzyme, converts fibrinogen, a protein substance, into fibrin, an insoluble protein that forms an intricate network of minute threadlike structures called fibrils and causes the blood plasma to gel. The blood cells and plasma are enmeshed in the network of fibrils to form the clot.
Blood Coagulation , ABO blood group & Rh factorSusmitaShaw3
1) The document summarizes blood coagulation, ABO blood group system, and Rh factor. It describes the process of haemostasis including vascular constriction, platelet plug formation, and blood clotting via the intrinsic and extrinsic pathways.
2) It explains the ABO blood group system which is based on the presence or absence of A and B antigens. The four blood groups are A, B, AB, and O depending on which antigens are present. It also describes the corresponding agglutinins (antibodies) found in each blood group.
3) The genetic inheritance of blood groups is discussed where the A, B, and O genes determine the antigens present. The Rh factor, a
This document discusses immunology, serology, and blood banking. It provides information on specimen collection and storage, the roles of antigens, immunogens, and antibodies, and various immunological tests including agglutination, lateral flow tests, and blood typing. It also covers blood banking procedures such as blood collection and storage, blood component preparation, and donor selection and deferral criteria. Key aspects of blood grouping and crossmatching are explained.
Erythropoietin (EPO) is a hormone produced primarily by the kidneys. It plays a key role in the production of red blood cells (RBCs), which carry oxygen from the lungs to the rest of the body.
The document summarizes the physiology of blood coagulation, including the five main components (vessels, platelets, coagulation factors, inhibitors, fibrinolysis) and how they work together in a complex system. It describes platelet activation and aggregation to form a platelet plug, coagulation factors that amplify to form a fibrin mesh to strengthen the clot, and fibrinolysis to prevent excessive clotting and allow blood to flow again. A balance is needed between coagulation and anticoagulation/fibrinolysis to control clotting.
This document discusses the treatment of anemia and the need for red blood cell substitutes. It begins by outlining the reasons to treat anemia and discusses the mortality risk of anemia versus the morbidity of red blood cell transfusions. Current possibilities for red blood cell substitutes are then summarized, including hemoglobin-based oxygen carriers (HBOCs) such as Hemopure, Polyheme, and Sanguinate. Toxicities of HBOCs like vasoconstriction and nitric oxide depletion are also noted. The document concludes by discussing protocols for managing severe anemia in the interim before fully developed red blood cell substitutes, and the potential of in vitro production of red blood cells as a future option.
Factor VIII (FVIII) is an essential blood-clotting protein, also known as anti-hemophilic factor (AHF). In humans, factor VIII is encoded by the F8 gene. Defects in this gene result in hemophilia A, a recessive X-linked coagulation disorder. ... The factor VIII gene produces two alternatively spliced transcripts
This document summarizes the cell-based model of coagulation. It describes coagulation as occurring in three overlapping phases: initiation, amplification, and propagation. In initiation, tissue factor activates factors VII and X. Amplification involves platelet activation and formation of complexes that generate a burst of thrombin. Propagation uses this thrombin to rapidly form a stable fibrin plug through fibrin and factor XIII. Control mechanisms like TFPI and natural anticoagulants prevent excess coagulation. Deficiencies help understand the model, as factor VII deficiency causes bleeding despite an intact intrinsic pathway, implicating its role in initiation.
The circulatory system transports blood throughout the body to deliver oxygen and nutrients to tissues and remove waste. It has three main functions: transportation, regulation, and protection. The circulatory system consists of the heart, blood vessels, and blood. The heart pumps blood through a closed system of arteries, capillaries and veins. Blood is composed of plasma and formed elements including red blood cells, white blood cells and platelets.
Blood component therapy and blood substitutes Himanshu Jangid
This document summarizes different types of blood products and transfusions. It discusses whole blood and its shelf life of 35 days when stored with CPDA-1. It also describes the production and storage of blood components like packed red blood cells, platelet concentrates, granulocytes and plasma derivatives. Key elements covered are donor screening, testing, storage conditions and guidelines for transfusion thresholds.
This document provides a summary of the history and process of blood transfusion from the 15th century to present day. It describes key historical figures and advances such as the discovery of blood groups by Landsteiner in 1901. The document outlines donor criteria, components of blood like red blood cells, plasma, platelets, and derivatives. It discusses transfusion indications, testing, and potential immune and non-immune mediated transfusion reactions.
1. Blood transfusions can be indicated for both elective and emergency situations such as anemia, hemorrhage, surgery, and trauma.
2. The ABO and Rh blood group systems are the most important to screen for due to the risk of hemolytic transfusion reactions from naturally occurring antibodies.
3. Whole blood can be stored for 35 days while components like packed red blood cells and platelets have shorter storage times and are preferred to minimize changes during storage.
Blood is considered a connective tissue because it has a matrix. ... Blood Tissue: Blood is a connective tissue that has a fluid matrix, called plasma, and no fibers. Erythrocytes (red blood cells), the predominant cell type, are involved in the transport of oxygen and carbon dioxide.
Blood coagulation, also known as hemostasis, is the process by which blood changes from a liquid to a solid gel-like substance. It involves three stages: vasoconstriction, formation of a platelet plug, and coagulation of blood. When a blood vessel is injured, a series of reactions are initiated through the intrinsic and extrinsic pathways, ultimately resulting in a cross-linked fibrin mesh that traps blood cells to form a clot. Coagulation is tightly regulated by several mechanisms to prevent excessive clotting. Deficiencies or defects in the coagulation cascade can result in bleeding disorders.
This document discusses the processes of hemostasis, thrombosis, and fibrinolysis. It defines key terms like blood clot, platelet, fibrin, coagulation cascade, and anticoagulants. The document describes the steps of primary hemostasis which involves platelet adhesion and activation at the site of injury. It also outlines the secondary hemostasis process known as the coagulation cascade that generates thrombin and ultimately forms a fibrin clot to stop bleeding. The roles of fibrinolysis and anticoagulant pathways in regulating clot formation are also summarized.
Blood can be separated into components to meet most transfusion needs while minimizing risks. Effective separation requires centrifugation based on differences in specific gravity of components. Common components prepared include packed red blood cells, platelet concentrates, fresh frozen plasma, and granulocyte concentrates. Preparation of blood components allows for optimal use of donated blood by providing only the required constituent to the patient in need.
The lymphatic system collects fluid that leaks from blood vessels into tissues and returns it to the circulatory system. Lymph vessels carry this fluid through lymph nodes, which filter the fluid and produce white blood cells, before returning it to the circulatory system via veins near the collarbone. Blood transports nutrients, oxygen, waste products, and more throughout the body. It is composed of plasma and blood cells including red blood cells, white blood cells, and platelets, each with distinct functions like oxygen transport, waste removal, and clotting. A person's blood type is determined by antigens on red blood cells, and the Rh factor is another important antigen that can cause complications during pregnancy if mother and child are incompatible.
This document discusses platelet function and disorders. It begins by describing platelet production, structure, and the key roles of platelets in hemostasis and thrombosis. It then examines the processes of platelet activation and aggregation. The document reviews methods to assess platelet function including bleeding time, aggregometry, and thromboelastography. It details several inherited disorders of platelet function like Bernard-Soulier syndrome and Glanzmann thrombasthenia. Finally, it covers acquired platelet dysfunctions from medications and treatments for platelet disorders.
This document discusses several books and concepts related to organizational leadership and structure in education. It summarizes Jim Collins' book "Good to Great" which identifies leadership styles of humility and discipline. It also discusses the importance of professional learning communities that allow teachers to collaborate. Additionally, it outlines John Maxwell's "21 Irrefutable Laws of Leadership" and the key rules around building relationships and developing future leaders. Finally, Edie Holcomb's book "Asking the Right Questions" is mentioned, focusing on implementing change through strategic planning.
The colonists achieved their goal of independence from Great Britain through several key events: the First Continental Congress organized militias in response to the crisis, the battles of Lexington and Concord marked the beginning of the Revolutionary War, and the Second Continental Congress appointed George Washington as commander and declared that war with Britain was necessary. Thomas Paine's influential pamphlet "Common Sense" encouraged declaring independence, and the Declaration of Independence was finally signed on July 4, 1776.
Coagulation: In medicine, the clotting of blood. The process by which the blood clots to form solid masses, or clots.
More than 30 types of cells and substances in blood affect clotting. The process is initiated by blood platelets. Platelets produce a substance that combines with calcium ions in the blood to form thromboplastin, which in turn converts the protein prothrombin into thrombin in a complex series of reactions. Thrombin, a proteolytic enzyme, converts fibrinogen, a protein substance, into fibrin, an insoluble protein that forms an intricate network of minute threadlike structures called fibrils and causes the blood plasma to gel. The blood cells and plasma are enmeshed in the network of fibrils to form the clot.
Blood Coagulation , ABO blood group & Rh factorSusmitaShaw3
1) The document summarizes blood coagulation, ABO blood group system, and Rh factor. It describes the process of haemostasis including vascular constriction, platelet plug formation, and blood clotting via the intrinsic and extrinsic pathways.
2) It explains the ABO blood group system which is based on the presence or absence of A and B antigens. The four blood groups are A, B, AB, and O depending on which antigens are present. It also describes the corresponding agglutinins (antibodies) found in each blood group.
3) The genetic inheritance of blood groups is discussed where the A, B, and O genes determine the antigens present. The Rh factor, a
This document discusses immunology, serology, and blood banking. It provides information on specimen collection and storage, the roles of antigens, immunogens, and antibodies, and various immunological tests including agglutination, lateral flow tests, and blood typing. It also covers blood banking procedures such as blood collection and storage, blood component preparation, and donor selection and deferral criteria. Key aspects of blood grouping and crossmatching are explained.
Erythropoietin (EPO) is a hormone produced primarily by the kidneys. It plays a key role in the production of red blood cells (RBCs), which carry oxygen from the lungs to the rest of the body.
The document summarizes the physiology of blood coagulation, including the five main components (vessels, platelets, coagulation factors, inhibitors, fibrinolysis) and how they work together in a complex system. It describes platelet activation and aggregation to form a platelet plug, coagulation factors that amplify to form a fibrin mesh to strengthen the clot, and fibrinolysis to prevent excessive clotting and allow blood to flow again. A balance is needed between coagulation and anticoagulation/fibrinolysis to control clotting.
This document discusses the treatment of anemia and the need for red blood cell substitutes. It begins by outlining the reasons to treat anemia and discusses the mortality risk of anemia versus the morbidity of red blood cell transfusions. Current possibilities for red blood cell substitutes are then summarized, including hemoglobin-based oxygen carriers (HBOCs) such as Hemopure, Polyheme, and Sanguinate. Toxicities of HBOCs like vasoconstriction and nitric oxide depletion are also noted. The document concludes by discussing protocols for managing severe anemia in the interim before fully developed red blood cell substitutes, and the potential of in vitro production of red blood cells as a future option.
Factor VIII (FVIII) is an essential blood-clotting protein, also known as anti-hemophilic factor (AHF). In humans, factor VIII is encoded by the F8 gene. Defects in this gene result in hemophilia A, a recessive X-linked coagulation disorder. ... The factor VIII gene produces two alternatively spliced transcripts
This document summarizes the cell-based model of coagulation. It describes coagulation as occurring in three overlapping phases: initiation, amplification, and propagation. In initiation, tissue factor activates factors VII and X. Amplification involves platelet activation and formation of complexes that generate a burst of thrombin. Propagation uses this thrombin to rapidly form a stable fibrin plug through fibrin and factor XIII. Control mechanisms like TFPI and natural anticoagulants prevent excess coagulation. Deficiencies help understand the model, as factor VII deficiency causes bleeding despite an intact intrinsic pathway, implicating its role in initiation.
The circulatory system transports blood throughout the body to deliver oxygen and nutrients to tissues and remove waste. It has three main functions: transportation, regulation, and protection. The circulatory system consists of the heart, blood vessels, and blood. The heart pumps blood through a closed system of arteries, capillaries and veins. Blood is composed of plasma and formed elements including red blood cells, white blood cells and platelets.
Blood component therapy and blood substitutes Himanshu Jangid
This document summarizes different types of blood products and transfusions. It discusses whole blood and its shelf life of 35 days when stored with CPDA-1. It also describes the production and storage of blood components like packed red blood cells, platelet concentrates, granulocytes and plasma derivatives. Key elements covered are donor screening, testing, storage conditions and guidelines for transfusion thresholds.
This document provides a summary of the history and process of blood transfusion from the 15th century to present day. It describes key historical figures and advances such as the discovery of blood groups by Landsteiner in 1901. The document outlines donor criteria, components of blood like red blood cells, plasma, platelets, and derivatives. It discusses transfusion indications, testing, and potential immune and non-immune mediated transfusion reactions.
1. Blood transfusions can be indicated for both elective and emergency situations such as anemia, hemorrhage, surgery, and trauma.
2. The ABO and Rh blood group systems are the most important to screen for due to the risk of hemolytic transfusion reactions from naturally occurring antibodies.
3. Whole blood can be stored for 35 days while components like packed red blood cells and platelets have shorter storage times and are preferred to minimize changes during storage.
Blood is considered a connective tissue because it has a matrix. ... Blood Tissue: Blood is a connective tissue that has a fluid matrix, called plasma, and no fibers. Erythrocytes (red blood cells), the predominant cell type, are involved in the transport of oxygen and carbon dioxide.
Blood coagulation, also known as hemostasis, is the process by which blood changes from a liquid to a solid gel-like substance. It involves three stages: vasoconstriction, formation of a platelet plug, and coagulation of blood. When a blood vessel is injured, a series of reactions are initiated through the intrinsic and extrinsic pathways, ultimately resulting in a cross-linked fibrin mesh that traps blood cells to form a clot. Coagulation is tightly regulated by several mechanisms to prevent excessive clotting. Deficiencies or defects in the coagulation cascade can result in bleeding disorders.
This document discusses the processes of hemostasis, thrombosis, and fibrinolysis. It defines key terms like blood clot, platelet, fibrin, coagulation cascade, and anticoagulants. The document describes the steps of primary hemostasis which involves platelet adhesion and activation at the site of injury. It also outlines the secondary hemostasis process known as the coagulation cascade that generates thrombin and ultimately forms a fibrin clot to stop bleeding. The roles of fibrinolysis and anticoagulant pathways in regulating clot formation are also summarized.
Blood can be separated into components to meet most transfusion needs while minimizing risks. Effective separation requires centrifugation based on differences in specific gravity of components. Common components prepared include packed red blood cells, platelet concentrates, fresh frozen plasma, and granulocyte concentrates. Preparation of blood components allows for optimal use of donated blood by providing only the required constituent to the patient in need.
The lymphatic system collects fluid that leaks from blood vessels into tissues and returns it to the circulatory system. Lymph vessels carry this fluid through lymph nodes, which filter the fluid and produce white blood cells, before returning it to the circulatory system via veins near the collarbone. Blood transports nutrients, oxygen, waste products, and more throughout the body. It is composed of plasma and blood cells including red blood cells, white blood cells, and platelets, each with distinct functions like oxygen transport, waste removal, and clotting. A person's blood type is determined by antigens on red blood cells, and the Rh factor is another important antigen that can cause complications during pregnancy if mother and child are incompatible.
This document discusses platelet function and disorders. It begins by describing platelet production, structure, and the key roles of platelets in hemostasis and thrombosis. It then examines the processes of platelet activation and aggregation. The document reviews methods to assess platelet function including bleeding time, aggregometry, and thromboelastography. It details several inherited disorders of platelet function like Bernard-Soulier syndrome and Glanzmann thrombasthenia. Finally, it covers acquired platelet dysfunctions from medications and treatments for platelet disorders.
This document discusses several books and concepts related to organizational leadership and structure in education. It summarizes Jim Collins' book "Good to Great" which identifies leadership styles of humility and discipline. It also discusses the importance of professional learning communities that allow teachers to collaborate. Additionally, it outlines John Maxwell's "21 Irrefutable Laws of Leadership" and the key rules around building relationships and developing future leaders. Finally, Edie Holcomb's book "Asking the Right Questions" is mentioned, focusing on implementing change through strategic planning.
The colonists achieved their goal of independence from Great Britain through several key events: the First Continental Congress organized militias in response to the crisis, the battles of Lexington and Concord marked the beginning of the Revolutionary War, and the Second Continental Congress appointed George Washington as commander and declared that war with Britain was necessary. Thomas Paine's influential pamphlet "Common Sense" encouraged declaring independence, and the Declaration of Independence was finally signed on July 4, 1776.
The document discusses two topics: the Cause and Effect of the X,Y,Z Affair and the Alien & Sedition Act. The Alien & Sedition Act limited the freedom of the Democratic-Republican party as many immigrants who supported the party, like French Americans, were impacted. It was argued that the Act gave the federal government too much power.
Matching Grants - A tool to strengthen fellowship & International GoodwillPrakash Saraswat
If you think that doing a Matching Grant simply as something to get the money, use it and forget to stay in touch with the partner thereafter...
...You’re missing the ‘’purpose’’ –
to strengthen fellowship and build International Goodwill through service
Ronald Reagan was a Republican politician who served as the 40th President of the United States from 1981 to 1989. He gained popularity with his conservative views and gave speeches supporting Barry Goldwater's 1964 presidential campaign. Reagan defeated incumbent Jimmy Carter in the 1980 election campaigning on a platform of tax cuts, reduced spending, and a stronger national defense. As president, Reagan implemented supply-side economic policies known as "Reaganomics" and advocated for a reduced role of government intervention in the economy. His presidency marked a conservative realignment in American politics and culture.
The Rotary Foundation's mission is to advance world understanding, goodwill, and peace through humanitarian projects. It is funded by voluntary contributions from Rotarians and friends. Through Foundation grants and programs, Rotarians can help fund clean water wells, environmental projects, and scholarships. The grants allow Rotarians to realize Rotary's goal of eradicating polio worldwide. The Future Vision plan focuses efforts in six areas to achieve greater impact. It introduces district and global grants to fund strategically focused, high-impact activities.
This document provides information about packaged grants available through The Rotary Foundation's Future Vision Plan. It discusses strategic partnerships that have been established with organizations like Aga Khan University, Mercy Ships, Oikocredit, and UNESCO-IHE to fund pre-designed global grant projects in areas like health, education, economic development, and water/sanitation. It provides details on applying for two packaged grant opportunities - one through Oikocredit to develop local entrepreneurs, and one for scholarships through the UNESCO-IHE partnership. Clubs must submit proposals for packaged grants that are reviewed on a first-come, first-served basis.
The colonists achieved their goal of independence from Great Britain through several key events: the First Continental Congress organized militias in response to the crisis, the battles of Lexington and Concord marked the beginning of the Revolutionary War, and the Second Continental Congress appointed George Washington as commander and declared that war with Britain was necessary. Thomas Paine's influential pamphlet "Common Sense" encouraged declaring independence, and the Declaration of Independence was finally signed on July 4, 1776.
The document appears to be instructions for an interactive game where the player helps aliens recover stolen spaceships. It guides the player through multiple levels requiring them to click on spaceships before time runs out. It also includes quiz questions to test the player's knowledge with feedback on correct and incorrect answers. The overarching goal is to complete all levels and recover the stolen spaceships to save the alien planet.
Progressive era reformers in the early 20th century sought to address social problems through four main goals: protecting social welfare, promoting moral improvement, creating economic reform, and fostering efficiency. Reform efforts included regulating working conditions, limiting child labor, securing worker's compensation, and directly electing U.S. senators to make government more responsive to citizens. Journalists known as "muckrakers" also exposed corruption in big business to promote reform.
The tensions between the colonies and Great Britain led to armed conflict in 1775. The First Continental Congress demanded rights from Britain. Armed conflict broke out at Lexington and Concord with the "shot heard 'round the world." The Second Continental Congress created the Continental Army to fight the British and named George Washington as Commander. Many colonists supported independence after Thomas Paine's "Common Sense" was published.
The document summarizes the economic development of the post-Civil War New South from the late 1800s to early 1900s. It describes the growth of industries like textiles, coal, steel production in Birmingham, and tobacco in Durham, North Carolina. It also discusses the rise of sharecropping and tenant farming, as well as the emergence of Jim Crow laws that enforced racial segregation and disenfranchisement of African Americans in the Southern states in this period.
The period after the War of 1812 saw the emergence of both nationalism and sectionalism in the United States. While President James Monroe's administration attempted to promote national unity during the "Era of Good Feelings," economic and demographic changes strengthened regional identities and tensions over the expansion of slavery grew with the Missouri Compromise of 1820. By the 1824 and 1828 presidential elections, partisanship had replaced the brief period of unified national spirit.
The Second Great Awakening led to the rise of African American churches in the early 19th century. This revivalism spread to the black community and converted many to Baptism and Methodism, leading to the formation of all-black churches primarily in the North. The African Methodist Episcopal Church had over 17,000 members by 1846. Joseph Smith founded the Church of Jesus Christ of Latter-day Saints in 1827 after announcing he had discovered golden plates containing the Book of Mormon. He gathered followers and tried to establish the City of Zion in Ohio, Missouri, and Illinois, facing persecution that culminated in Smith's murder in 1844. Brigham Young then led Mormons westward to Utah in 1846
The document discusses 19th century reform movements and utopian communities in America. It outlines the growth of the middle class, the Second Great Awakening religious revival, and middle-class reform movements like temperance and efforts to stop prostitution. It also describes several utopian communities established in the 1800s including New Harmony, Brook Farm, and the Oneida Community, each with different ideals but seeking social improvement through new societies.
The Rotary Foundation was established in 1917 as an endowment fund by Rotary International President Arch C. Klumph. It was reorganized in 1929 into the structure it has today. The mission of the Foundation is to enable Rotarians to advance world understanding, goodwill, and peace through humanitarian, educational, and cultural exchange projects. It supports Rotarian activities worldwide through program grants and scholarships. Major programs include PolioPlus for global polio eradication, peace centers, and Foundation grants.
The document discusses the Second Great Awakening period from 1820-1840s in America and the social reforms that arose from it. The Second Great Awakening was a period of intense religious revivalism that spread evangelical Protestantism. It helped foster reforms around temperance, education, women's rights, abolitionism and more. Figures like Charles Finney promoted the new revivalist style of emotionally charged preaching that helped spread evangelical Christianity and shape society in this period of rapid social and economic change in America.
1. hemodyanamics normal hemostasis- dr. sinhasan- mdzahkciapm
1. The document describes the components of normal hemostasis including the endothelium, platelets, plasma coagulation factors, and the fibrinolytic system.
2. It explains the process of hemostasis including vasoconstriction at the site of injury, platelet adhesion and aggregation during primary hemostasis, and fibrin deposition during secondary hemostasis via the coagulation cascade.
3. The document discusses the properties of the endothelium, noting it can be both prothrombotic and antithrombotic depending on the balance between procoagulant and anticoagulant factors.
Coagulation: In medicine, the clotting of blood. The process by which the blood clots to form solid masses, or clots.
More than 30 types of cells and substances in blood affect clotting. The process is initiated by blood platelets. Platelets produce a substance that combines with calcium ions in the blood to form thromboplastin, which in turn converts the protein prothrombin into thrombin in a complex series of reactions. Thrombin, a proteolytic enzyme, converts fibrinogen, a protein substance, into fibrin, an insoluble protein that forms an intricate network of minute threadlike structures called fibrils and causes the blood plasma to gel. The blood cells and plasma are enmeshed in the network of fibrils to form the clot.
This document discusses coagulation factors and blood clotting. It defines coagulation as the process where blood loses fluidity and forms a jelly-like clot. Thirteen coagulation factors are involved in a cascade of reactions to form a clot. The cascade involves the formation of prothrombin activator through the intrinsic and extrinsic pathways, followed by the conversion of prothrombin to thrombin and fibrinogen to fibrin. Deficiencies in specific factors can cause bleeding disorders like hemophilia. The clot then undergoes retraction and may be broken down through fibrinolysis.
Dental procedures can have serious consequences for patients with bleeding disorders, possibly resulting in severe hemorrhage or death. Laboratory tests help evaluate coagulation disorders and bleeding risks, including platelet count, bleeding time, PT/INR, aPTT, and tests for factors, fibrin degradation products, and capillary fragility. Treatment depends on the specific disorder or condition, and may include replacement of platelets, coagulation factors, cryotherapy, laser ablation, or medications like tranexamic acid, desmopressin, corticosteroids, or thrombopoietin agents.
1. The document discusses hemostasis and coagulation, including the three major systems involved: the vessel wall, platelets, and the coagulation cascade.
2. It describes the properties of the endothelium that promote both antithrombosis and prothrombosis, as well as the platelet response to different agonists.
3. The coagulation cascade and fibrinolysis are summarized, along with physiologic inhibitors such as antithrombin III and pathologies such as disseminated intravascular coagulation.
The document discusses various blood disorders that affect red blood cells, including different types of anemia. It describes iron-deficiency anemia, which can be caused by low iron intake or blood loss. Anemia of chronic disease is common in people with kidney disease or other chronic illnesses. Pernicious anemia results from a vitamin B12 deficiency due to problems absorbing the vitamin. Aplastic anemia occurs when the bone marrow does not produce enough red blood cells or other blood cells.
9-Coagulation mechanism (1).pptx HD ffuggSriDharshan5
The coagulation mechanism involves a balance between procoagulant and anticoagulant factors that promote or inhibit clotting. The coagulation cascade involves intrinsic and extrinsic pathways that activate thrombin, which converts fibrinogen to fibrin to form a blood clot. Fibrinolysis breaks down fibrin clots using plasmin. Natural anticoagulants like thrombomodulin, antithrombin III, and heparin regulate clot formation. Disturbances can lead to bleeding disorders or hypercoagulability.
Blood coagulation is a complex process involving multiple coagulation factors that activate each other in a cascade. This leads to the conversion of prothrombin to thrombin which then converts fibrinogen to fibrin to form a blood clot. Coagulation is regulated by a balance of procoagulant and anticoagulant factors. Disturbances can result in bleeding disorders or hypercoagulability.
Anticoagulation in diagnostic and interventional procedure and monitoring a...Deb Boruah
The document discusses anticoagulation in diagnostic and interventional procedures. It describes the three mechanisms of blood clotting - vascular spasm, platelet plug formation, and blood clotting. It then discusses the blood coagulation cascade and mechanisms of heparin and low molecular weight heparins as anticoagulants. It also covers monitoring of anticoagulation therapy, including tests for heparin, warfarin, and antiplatelet drugs.
Hemostasis is the process of stopping bleeding through vascular spasms, platelet plug formation, and coagulation. Key events include vasoconstriction, platelet aggregation, thromboxane A2 release, fibrinogen conversion to fibrin strands, and clot stabilization. Clot retraction and repair occur through platelet contraction and growth factor release. Fibrinolysis removes unneeded clots. Factors that limit clotting include antithrombin III and protein C. Disorders include deep vein thrombosis and hemophilia.
Platelets play a key role in hemostasis through adhesion, activation, and aggregation at the site of vascular injury to form a platelet plug. The coagulation cascade then forms a blood clot through a series of coagulation factor activations. This process is regulated by anti-coagulation mechanisms including thrombomodulin and the fibrinolytic system. Abnormalities can cause excessive bleeding from issues like thrombocytopenia or vitamin K deficiency, or excessive clotting from conditions like deep vein thrombosis. Laboratory tests evaluate platelet count and function as well as coagulation factor levels.
Platelets are disk-like cell fragments that originate from megakaryocytes and play a key role in hemostasis. When a blood vessel is damaged, platelets adhere to the site of injury and aggregate to form a platelet plug. This triggers the coagulation cascade, resulting in a fibrin clot that further strengthens the platelet plug. The clot then contracts through actin and myosin in the platelets. Over time, plasmin dissolves the clot through fibrinolysis, restoring blood flow in the vessel. A balance of pro-coagulant and anticoagulant factors normally maintains blood in a fluid state.
This chapter discusses the composition and functions of blood. Blood transports gases, nutrients, waste products, and regulatory molecules. It is composed of plasma and formed elements, including erythrocytes, leukocytes, and thrombocytes. Erythrocytes contain hemoglobin and transport oxygen, while leukocytes help fight infection. Platelets help form blood clots to prevent blood loss from damaged vessels. Blood grouping involves antigens and antibodies that determine blood type.
Blood homeostasis depends on the continual transport of components to and from cells. The composition of blood includes plasma, which makes up 55% of blood, and formed elements such as red blood cells, white blood cells, and platelets, which make up the remaining 45%. Blood disorders can involve abnormalities in any of the formed elements, including anemias that decrease oxygen-carrying capacity, leukocyte disorders like leukemia, and clotting disorders such as hemophilia or thrombosis.
This document discusses hypercoagulable states and normal hemostasis. It defines hypercoagulability and outlines the types, causes, and laboratory tests used to identify hypercoagulable states. Normal hemostasis relies on a balance between the coagulation cascade, fibrinolysis, and natural anticoagulants. Hypercoagulability results from disturbances in these systems that can be hereditary, such as Factor V Leiden, or acquired through medical conditions, medications, or lifestyle factors. Laboratory tests evaluate natural anticoagulants, fibrinolysis, coagulation activation markers, and genetic mutations to identify hypercoagulable states.
This document provides an overview of hemostasis and coagulation. It begins with objectives to appreciate the clinical importance, basic chemistry of mediators, and physiology of hemostasis. It then outlines the topics to be covered, including an introduction, definitions, prevalence of coagulation disorders, components of hemostasis, basic chemistry of coagulation factors, the physiology including the three pathways (initiation, amplification and propagation), regulation through inhibition of coagulation and fibrinolysis, relevant tests, factors affecting test results, clinical correlates, and a concluding summary.
Thrombocytopenia is most frequently encountered Hematological problem in hospitalized patients. The most common causes and differential diagnosis of In-patient and Outpatient presentations of Thrombocytopenia is discussed here. Useful for Internal Medicine Boards . Archer Internal Medicine Board review lectures will be released soon.
The document discusses blood coagulation and factors involved. It explains that coagulation depends on a balance between procoagulant and anticoagulant factors. The intrinsic and extrinsic pathways activate thrombin which converts fibrinogen to fibrin to form a blood clot meshwork. Coagulation factors I through XIII are involved. Conditions that can cause excessive bleeding include vitamin K deficiency, hemophilia, and thrombocytopenia.
This document provides an overview of topics related to hematology and the history and pathophysiology of platelets. It discusses:
1) Early studies identifying platelets as distinct blood components arising from megakaryocytes.
2) Thrombopoiesis and the role of thrombopoietin in platelet production.
3) Causes of thrombocytopenia including decreased production, increased destruction, pseudo-thrombocytopenia, and altered platelet distribution. Specific conditions like ITP, DIC, and TTP are mentioned.
3) Strategies for evaluating and classifying the severity of thrombocytopenia.
The document provides a high-level summary of key
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
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Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Mercurius is named after the roman god mercurius, the god of trade and science. The planet mercurius is named after the same god. Mercurius is sometimes called hydrargyrum, means ‘watery silver’. Its shine and colour are very similar to silver, but mercury is a fluid at room temperatures. The name quick silver is a translation of hydrargyrum, where the word quick describes its tendency to scatter away in all directions.
The droplets have a tendency to conglomerate to one big mass, but on being shaken they fall apart into countless little droplets again. It is used to ignite explosives, like mercury fulminate, the explosive character is one of its general themes.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
1. MCP-1 AND IL-8 EXPRESSION
BY MONOCYTES IN CLOTS
Paola A. Arias-Mendoza, MS1
University of Puerto Rico,
Medical Sciences Campus
Robert Campbell, Ph.D.
Andrew S. Weyrich, Ph.D.
Program in Molecular Medicine
University of Utah
2. INTRODUCTION
• Cardiovascular Disease is the leading cause of death in US.
• Arterial thrombosis – Myocardial infarction and stroke
accounted for 37% of all deaths in 2007.
• Venous thrombosis – Effects more than a million a year
with 30% mortality within the first 30 days.
30. BACKGROUND
• Activated platelets interact with monocytes promoting chemokine secretion
involved in inflammatory response. (A.S. Weyrich 1996)
• Monocyte Chemotactic Protein 1 (MCP-1)
• Released by monocytes after induction by RANTES and P-selectin
expressed by platelets.
• Interleukin-8 (IL-8) also “neutrophil chemotatic factor”
• Known chemokine and angiogenic factor
• IL-8 and MCP-1 both needed for migration and proliferation of leukocytes in
subendothelial layers (Z. Franks 2010)
• IL-8 and MCP-1 have been found elevated in patients with stroke ( Z. Franks 2010)
31. IN VITRO SYSTEM
Form clot from donors plasma
Add 20 mM CaCl2 and tissue factor
Monocytes or Monocytes + Allow clot to form for 30 minutes
platelets
Overlay clot with monocytes or
Plasma Clot monocytes with platelets
Collect supernatant at designated
times and analyze for different
cytokines
32. BACKGROUND
120000
100000
S Counts per Minutes
80000
• Plasma Clots promotes an
increase in the synthesis of 60000
proteins. 40000
35
20000
0
NT IIa LPS Clot
33. RESULTS
IL‐8 MCP‐1
DAPI = Blue, CD14 = Green, IL‐8 or MCP‐1 = RED
34. OBJECTIVE
• Characterize MCP-1 and IL-8 mRNA expression in
monocytes associated with clots.
35. MATERIALS AND METHODS
• Blood peripheral monocytes isolation
• In vitro Clot system experiments
• RNA Isolation
• cDNA Preparation
• Real Time PCR
37. SUMMARY
• MCP-1 and IL-8 mRNA and protein are increased in monocytes
associated with clots
• Our data suggest clinicians should consider the inflammatory
consequences of thrombi in patients. Treatments focused on the
inflammatory response may results in better outcomes.
• Future Direction:
• Identification of other chemokines and other inflammatory genes.
• Determine mechanism of how clots induce inflammatory
response.
38. ACKNOWLEDGEMENTS
• PI: Andrew S. Weyrich, Ph.D.
• Mentor: Robert A. Campbell, Ph.D.
• Medical Research Program At University of Utah
• Janet Basset
• “Summer Family”
39. ACKNOWLEDGEMENTS
• PI: Andrew S. Weyrich, Ph.D.
• Mentor: Robert A. Campbell, Ph.D.
• Medical Research Program At University of Utah
• Janet Basset
• “Summer Family”
Editor's Notes
\n
Within those we found coagulation disorders like AT responsable for heart attacks and strokes wich...\nAlso VT . In Dr. Weyrich’s Lab we investigates the coagulation process and its associated inflammation responses in order to unsdestand such diseases.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
For those unfamiliar with the coagulation process i will try to explained in a simple way. First you have your blood in vessels and all its components like RBC, WBC, Platelets, Coagulations Factors: importants ones: Thombin and Fibrinogen. > When you get and injury in one of your vessels which happens many times each day, platelets recognizes some of the component in the subendothelial exposed layer and they aggregated forming a platelet plug, then they start secreting coagulation factors that leds to the activation of Thombin. Thrombin causes polymerization of fibrinogen molecules into fibrin fibers forming a meshwork that entraps blood cells, platelets and plasma, that is a clot, sealing your vessels. Monocytes interact with the clot, this led an inflammatory response that in our lab we are interested in. Led to Associated inflammatory response with the clot.\n
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Platelets Pour Plasma \n
Recently in our lab, using an in vitro clot system in which monocytes are exposed to clot removing the platelets, an increased in protein synthesis have been identified.\n
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My colaboration for the summer is the evaluation of the gene expression/ The goal of my 6 weeks project\n