Bolsheviks

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https://en.wikipedia.org/wiki/Bolsheviks

1920 Bolshevik Party meeting: sitting (from left) are Enukidze, Kalinin, Bukharin, Tomsky, Lashevich, Kamenev, Preobrazhensky, Serebryakov, Lenin and Rykov

The Bolsheviks, also known in English as the Bolshevists, were a radical far-left Marxist faction founded by Vladimir Lenin and Alexander Bogdanov that split from the Menshevik faction of the Marxist Russian Social Democratic Labour Party (RSDLP), a revolutionary socialist political party formed in 1898, at its Second Party Congress in 1903.

After forming their own party in 1912, the Bolsheviks took power in Russia in November 1917, overthrowing the liberal Provisional Government of Alexander Kerensky, and became the only ruling party in the subsequent Soviet Russia and its successor state, the Soviet Union. They considered themselves the leaders of the revolutionary working class of Russia. Their beliefs and practices were often referred to as Bolshevism.

History of the split

Lenin's ideology in What Is to Be Done?

Bolshevik, Boris Kustodiev, 1920

Lenin's political pamphlet What Is to Be Done?, which Lenin wrote in 1901 and published in 1902, helped to precipitate the split. In Germany, the book was published in 1902; but in Russia, strict censorship outlawed its publication and distribution. One of the main points of Lenin's writing was that a revolution can only be achieved by the strong leadership of the masses by one person, or by a very select few, who would dedicate their entire lives to the cause, although after the proposed revolution had successfully overthrown the government, this strong leadership would relinquish power to allow socialism to fully develop. Lenin said that if professional revolutionaries did not maintain control over the workers, then they would lose sight of the party's objective and adopt opposing beliefs, even abandon the revolution entirely.

The pamphlet also showed that Lenin's view of a socialist intelligentsia was not in line with Marxist theory, which also created some party unrest. For example, Lenin agreed with the Marxist idea of eliminating social classes, but his vision of a future society encompassed visible distinctions between those in politics and the common worker. Most party members considered unequal treatment of workers immoral and were loyal to the idea of a completely classless society. This pamphlet also showed that Lenin opposed another group of reformers, known as "Economists", who were for economic reform while leaving the government relatively unchanged and who, in Lenin's view, failed to recognize the importance of uniting the working population behind the party's cause.

2nd party congress

At the 2nd Congress of the RSDLP, which was held in Brussels and then London during August 1903, Lenin and Julius Martov disagreed over the party membership rules. Lenin, who was supported by Plekhanov, wanted to limit membership to those who supported the party full-time and worked in complete obedience to the elected party leadership. Martov wanted to extend membership to anyone "who recognises the Party Programme and supports it by material means and by regular personal assistance under the direction of one of the party’s organisations". Lenin believed his plan would develop a core group of professional revolutionaries who would devote their full time and energy towards developing the party into an organization capable of leading a successful workers' revolution against the Tsarist autocracy.

The base of active and experienced members would be the recruiting ground for this professional core. Sympathizers would be left outside and the party would be organised based on the concept of democratic centralism. Martov, until then a close friend of Lenin, agreed with him that the core of the party should consist of professional revolutionaries, but he argued that party membership should be open to sympathizers, revolutionary workers, and other fellow travellers. The two had disagreed on the issue as early as March–May 1903, but it was not until the Congress that their differences became irreconcilable and split the party. At first, the disagreement appeared to be minor and inspired by personal conflicts. For example, Lenin's insistence on dropping less active editorial board members from Iskra or Martov's support for the Organizing Committee of the Congress which Lenin opposed. The differences grew and the split became irreparable.

Internal unrest also arose over the political structure that was best suited for Soviet power. As discussed in What Is To Be Done?, Lenin firmly believed that a rigid political structure was needed to effectively initiate a formal revolution. This idea was met with opposition from once close followers, including Martov, Georgy Plekhanov, Leon Trotsky, and Pavel Axelrod. Plekhanov and Lenin's major dispute arose addressing the topic of nationalizing land or leaving it for private use. Lenin wanted to nationalize to aid in collectivization whereas Plekhanov thought worker motivation would remain higher if individuals were able to maintain their own property. Those who opposed Lenin and wanted to continue on the Marxist path towards complete socialism and disagreed with his strict party membership guidelines became known as "softs" while Lenin supporters became known as "hards".

Some of the factionalism could be attributed to Lenin's steadfast belief in his own opinion and what was described by Plekhanov as Lenin's inability to "bear opinions which were contrary to his own" and loyalty to his own self-envisioned utopia. Lenin was seen even by fellow party members as being so narrow-minded and unable to accept criticism that he believed that anyone who didn't follow him was his enemy. Leon Trotsky, one of Lenin's fellow revolutionaries, compared Lenin in 1904 to the French revolutionary Maximilien Robespierre.

Origins of Bolshevik and Menshevik

The two factions were originally known as "hard" (Lenin's supporters) and "soft" (Martov's supporters), but the terminology soon changed to "Bolsheviks" and "Mensheviks", from the Russian bolshinstvo ("majority") and menshinstvo ("minority"). In the Second Party Congress vote, the Bolsheviks won votes on the majority of important issues, hence the name. On the other hand, Martov's supporters won the vote concerning the question of party membership. Neither Lenin nor Martov had a firm majority throughout the Congress as delegates left or switched sides. In the end, the Congress was evenly split between the two factions.

From 1907 on, English language articles sometimes used the term "Maximalist" for "Bolshevik" and "Minimalist" for "Menshevik", which proved confusing since there was also a "Maximalist" faction within the Russian Socialist Revolutionary Party in 1904–1906 (which after 1906 formed a separate Union of Socialists-Revolutionaries Maximalists) and then again after 1917.

The Bolsheviks ultimately became the Communist Party of the Soviet Union. The Bolsheviks, or Reds, came to power in Russia during the October Revolution phase of the Russian Revolution of 1917 and founded the Russian Soviet Federative Socialist Republic (RSFSR). With the Reds defeating the Whites and others during the Russian Civil War of 1917–1922, the RSFSR became the chief constituent of the Soviet Union (USSR) in December 1922.

Demographics of the two factions

The average party member was very young. In 1907, 22% of Bolsheviks were under 20, 37% were 20–24 and 16% were 25–29. By 1905, 62% of the members were industrial workers (3% of the population in 1897). 22% of Bolsheviks were gentry (1.7% of the total population), 38% were uprooted peasants, compared with 19% and 26% for the Mensheviks. In 1907, 78.3% of the Bolsheviks were Russian and 10% were Jewish (34% and 20% for the Mensheviks). Total membership was 8,400 in 1905, 13,000 in 1906 and 46,100 by 1907 (8,400, 18,000 and 38,200 for the Mensheviks). By 1910, both factions together had fewer than 100,000 members.

Beginning of the 1905 Revolution (1903–1905)

The two factions were in a state of flux in 1903–1904 with many members changing sides. The founder of Russian Marxism, Georgy Plekhanov, who at first allied himself with Lenin and the Bolsheviks, had parted ways with them by 1904. Trotsky at first supported the Mensheviks, but he left them in September 1904 over their insistence on an alliance with Russian liberals and their opposition to a reconciliation with Lenin and the Bolsheviks. He remained a self-described "non-factional social democrat" until August 1917, when he joined Lenin and the Bolsheviks, as their positions resembled his and he came to believe that Lenin was right on the issue of the party.

All but one member of the RSDLP Central Committee were arrested in Moscow in early 1905. The remaining member, with the power of appointing a new committee, was won over by the Bolsheviks.

The lines between the Bolsheviks and the Mensheviks hardened in April 1905 when the Bolsheviks held a Bolsheviks-only meeting in London, which they called the 3rd Party Congress. The Mensheviks organised a rival conference and the split was thus finalized.

The Bolsheviks played a relatively minor role in the 1905 Revolution and were a minority in the Saint Petersburg Soviet of Workers' Deputies led by Trotsky. However, the less significant Moscow Soviet was dominated by the Bolsheviks. These Soviets became the model for those formed in 1917.

Mensheviks (1906–1907)

As the Russian Revolution of 1905 progressed, Bolsheviks, Mensheviks, and smaller non-Russian social democratic parties operating within the Russian Empire attempted to reunify at the 4th (Unification) Congress of the RSDLP held in April 1906 at Folkets hus, Norra Bantorget, in Stockholm. When the Mensheviks made an alliance with the Jewish Bund, the Bolsheviks found themselves in a minority.

However, all factions retained their respective factional structure and the Bolsheviks formed the Bolshevik Centre, the de facto governing body of the Bolshevik faction within the RSDLP. At the Fifth Congress held in London in May 1907, the Bolsheviks were in the majority, but the two factions continued functioning mostly independently of each other.

Split between Lenin and Bogdanov (1908–1910)

Tensions had existed between Lenin and Alexander Bogdanov from as early as 1904. Lenin had fallen out with Nikolai Valentinov after Valentinov had introduced him to Ernst Mach's Empiriocriticism, a viewpoint that Bogdanov had been exploring and developing as Empiriomonism. Having worked as co-editor with Plekhanov on Zarya, Lenin had come to agree with the Valentinov's rejection of Bogdanov's Empiriomonism. With the defeat of the revolution in mid-1907 and the adoption of a new, highly restrictive election law, the Bolsheviks began debating whether to boycott the new parliament known as the Third Duma. Lenin, Grigory Zinoviev, Lev Kamenev, and others argued for participating in the Duma while Bogdanov, Anatoly Lunacharsky, Mikhail Pokrovsky, and others argued that the social democratic faction in the Duma should be recalled. The latter became known as "recallists" (otzovists in Russian). A smaller group within the Bolshevik faction demanded that the RSDLP central committee should give its sometimes unruly Duma faction an ultimatum, demanding complete subordination to all party decisions. This group became known as "ultimatists" and was generally allied with the recallists.

With most Bolshevik leaders either supporting Bogdanov or undecided by mid-1908 when the differences became irreconcilable, Lenin concentrated on undermining Bogdanov's reputation as a philosopher. In 1909, he published a scathing book of criticism entitled Materialism and Empirio-criticism (1909), assaulting Bogdanov's position and accusing him of philosophical idealism. In June 1909, Bogdanov proposed the formation of Party Schools as Proletarian Universities at a Bolshevik mini-conference in Paris organised by the editorial board of the Bolshevik magazine Proletary. However, this proposal was not adopted and Lenin tried to expel Bogdanov from the Bolshevik faction. Bogdanov was then involved with setting up Vpered, which ran the Capri Party School from August to December 1909.

Final attempt at party unity (1910)

With both Bolsheviks and Mensheviks weakened by splits within their ranks and by Tsarist repression, the two factions were tempted to try to re-unite the party. In January 1910, Leninists, recallists, and various Menshevik factions held a meeting of the party's Central Committee in Paris. Kamenev and Zinoviev were dubious about the idea; but under pressure from conciliatory Bolsheviks like Victor Nogin, they were willing to give it a try.

One of the underlying reasons that prevented any reunification of the party was the Russian police. The police were able to infiltrate both parties' inner circles by sending in spies who then reported on the opposing party's intentions and hostilities. This allowed the tensions to remain high between the Bolsheviks and Mensheviks and helped prevent their uniting. 

Lenin was firmly opposed to any re-unification but was outvoted within the Bolshevik leadership. The meeting reached a tentative agreement, and one of its provisions was to make Trotsky's Vienna-based Pravda a party-financed central organ. Kamenev, Trotsky's brother-in-law who was with the Bolsheviks, was added to the editorial board; but the unification attempts failed in August 1910 when Kamenev resigned from the board amid mutual recriminations.

Forming a separate party (1912)

Leon Trotsky, Vladimir Lenin and Lev Kamenev

The factions permanently broke relations in January 1912 after the Bolsheviks organised a Bolsheviks-only Prague Party Conference and formally expelled Mensheviks and recallists from the party. As a result, they ceased to be a faction in the RSDLP and instead declared themselves an independent party, called Russian Social Democratic Labour Party (Bolsheviks) – or RSDLP(b). Unofficially, the party has been referred to as the Bolshevik Party. Throughout the 20th century, the party adopted a number of different names. In 1918, RSDLP(b) became All-Russian Communist Party (Bolsheviks) and remained so until 1925. From 1925–1952, the name was All-Union Communist Party (Bolsheviks) and from 1952–1991 Communist Party of the Soviet Union. 

As the party split became permanent, further divisions became evident. One of the most notable differences was how each faction decided to fund its revolution. The Mensheviks decided to fund their revolution through membership dues while Lenin often resorted to more drastic measures since he required a higher budget. One of the common methods the Bolsheviks used was committing bank robberies, one of which, in 1907, resulted in the party getting over 250,000 roubles, which is the equivalent of about $125,000. Bolsheviks were in constant need of money because Lenin practised his beliefs, expressed in his writings, that revolutions must be led by individuals who devote their entire lives to the cause. As compensation, he rewarded them with salaries for their sacrifice and dedication. This measure was taken to help ensure that the revolutionaries stayed focused on their duties and motivated them to perform their jobs. Lenin also used the party money to print and copy pamphlets which were distributed in cities and at political rallies in an attempt to expand their operations. Both factions received funds through donations from wealthy supporters.

The elections to the Russian Constituent Assembly took place in November 1917 in which the Bolsheviks came second with 23.9% of the vote and dissolved the Assembly in January 1918

 

Further differences in party agendas became evident as the beginning of World War I loomed near. Joseph Stalin was especially eager for the start of the war, hoping that it would turn into a war between classes or essentially a Russian Civil War. This desire for war was fuelled by Lenin's vision that the workers and peasants would resist joining the war effort and therefore be more compelled to join the socialist movement. Through the increase in support, Russia would then be forced to withdraw from the Allied powers in order to resolve her internal conflict. Unfortunately for the Bolsheviks, Lenin's assumptions were incorrect. Despite his and the party's attempts to push for a civil war through involvement in two conferences in 1915 and 1916 in Switzerland, the Bolsheviks were in the minority in calling for a ceasefire by the Russian Army in World War I.

Although the Bolshevik leadership had decided to form a separate party, convincing pro-Bolshevik workers within Russia to follow suit proved difficult. When the first meeting of the Fourth Duma was convened in late 1912, only one out of six Bolshevik deputies, Matvei Muranov (another one, Roman Malinovsky, was later exposed as an Okhrana agent), voted on 15 December 1912 to break from the Menshevik faction within the Duma. The Bolshevik leadership eventually prevailed, and the Bolsheviks formed their own Duma faction in September 1913.

One final difference between the Bolsheviks and Mensheviks was how ferocious and tenacious the Bolshevik party was in order to achieve its goals, although Lenin was open minded to retreating from political ideals if he saw the guarantee of long-term gains benefiting the party. This practice was seen in the party's trying to recruit peasants and uneducated workers by promising them how glorious life would be after the revolution and granting them temporary concessions.

In 1918, the party renamed itself the Russian Communist Party (Bolsheviks) at Lenin's suggestion. In 1925, this was changed to All-Union Communist Party (Bolsheviks). At the 19th Party Congress in 1952 the Bolshevik Party was renamed the Communist Party of the Soviet Union at Stalin's suggestion.

Non-Russian/Soviet groups having used the name "Bolshevik"

• Bangladesh: Maoist Bolshevik Reorganisation Movement of the Purba Banglar Sarbahara Party
• Burkina Faso: Burkinabé Bolshevik Party
• India: Bolshevik Party of India
• India/Sri Lanka: Bolshevik-Leninist Party of India, Ceylon and Burma
• India: Revolutionary Socialist Party (Bolshevik)
• Mexico: Bolshevik Communist Party
• Senegal: Bolshevik Nuclei
• Sri Lanka: Bolshevik Samasamaja Party
• Turkey: Bolshevik Party (North Kurdistan – Turkey)

Derogatory usage of "Bolshevik"

"Down with Bolshevism. Bolshevism brings war and destruction, hunger and death", anti-Bolshevik German propaganda, 1919

 

"Bolo" was a derogatory expression for Bolsheviks used by British service personnel in the North Russian Expeditionary Force which intervened against the Red Army during the Russian Civil War. Adolf Hitler, Joseph Goebbels and other Nazi leaders used it in reference to the worldwide political movement coordinated by the Comintern. During the days of the Cold War in the United Kingdom, labour union leaders and other leftists were sometimes derisively described as "Bolshies". The usage is roughly equivalent to the term "commie", "Red", or "pinko" in the United States during the same period. The term "Bolshie" later became a slang term for anyone who was rebellious, aggressive, or truculent.

Coagulation

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Coagulation 

Coagulation
Blood coagulation pathways in vivo showing the central role played by thrombin
Health	Beneficial

Coagulation, also known as clotting, is the process by which blood changes from a liquid to a gel, forming a blood clot. It potentially results in hemostasis, the cessation of blood loss from a damaged vessel, followed by repair. The mechanism of coagulation involves activation, adhesion and aggregation of platelets, as well as deposition and maturation of.

Coagulation begins almost instantly after an injury to the blood vessel has damaged the endothelium lining the blood vessel. Exposure of blood to the subendothelial space initiates two processes: changes in platelets, and the exposure of subendothelial tissue factor to plasma factor VII, which ultimately leads to cross-linked fibrin formation. Platelets immediately form a plug at the site of injury; this is called primary hemostasis. Secondary hemostasis occurs simultaneously: additional coagulation (clotting) factors beyond factor VII  respond in a cascade to form fibrin strands, which strengthen the platelet plug.

Disorders of coagulation are disease states which can result in hemorrhage, bruising, or thrombosis.

Coagulation is highly conserved throughout biology. In all mammals, coagulation involves both a cellular (platelet) and a protein (coagulation factor) component. The system in humans has been the most extensively researched and is the best understood.

Physiology

The interaction of vWF and GP1b alpha. The GP1b receptor on the surface of platelets allows the platelet to bind to vWF, which is exposed upon damage to vasculature. The vWF A1 domain (yellow) interacts with the extracellular domain of GP1ba (blue).

Platelet activation

When the endothelium is damaged, the normally isolated, underlying collagen is exposed to circulating platelets, which bind directly to collagen with collagen-specific glycoprotein Ia/IIa surface receptors. This adhesion is strengthened further by von Willebrand factor (vWF), which is released from the endothelium and from platelets; vWF forms additional links between the platelets' glycoprotein Ib/IX/V and A1 domain. This localization of platelets to the extracellular matrix promotes collagen interaction with platelet glycoprotein VI. Binding of collagen to glycoprotein VI triggers a signaling cascade that results in activation of platelet integrins. Activated integrins mediate tight binding of platelets to the extracellular matrix. This process adheres platelets to the site of injury.

Activated platelets release the contents of stored granules into the blood plasma. The granules include ADP, serotonin, platelet-activating factor (PAF), vWF, platelet factor 4, and thromboxane A₂ (TXA₂), which, in turn, activate additional platelets. The granules' contents activate a G_q-linked protein receptor cascade, resulting in increased calcium concentration in the platelets' cytosol. The calcium activates protein kinase C, which, in turn, activates phospholipase A₂ (PLA₂). PLA₂ then modifies the integrin membrane glycoprotein IIb/IIIa, increasing its affinity to bind fibrinogen. The activated platelets change shape from spherical to stellate, and the fibrinogen cross-links with glycoprotein IIb/IIIa aid in aggregation of adjacent platelets (completing primary hemostasis).

Coagulation cascade

The classical blood coagulation pathway

 

Modern coagulation pathway. Hand-drawn composite from similar drawings presented by Professor Dzung Le, MD, PhD, at UCSD Clinical Chemistry conferences on 14 and 21 October 2014. Original schema from Introduction to Hematology by Samuel I. Rapaport. 2nd edition;Lippencott:1987. Dr Le added the factor XI portion based on a paper from about year 2000. Dr. Le's similar drawings presented the development of this cascade over 6 frames, like a comic.

 

The coagulation cascade of secondary hemostasis has two initial pathways which lead to fibrin formation. These are the contact activation pathway (also known as the intrinsic pathway), and the tissue factor pathway (also known as the extrinsic pathway), which both lead to the same fundamental reactions that produce fibrin. It was previously thought that the two pathways of coagulation cascade were of equal importance, but it is now known that the primary pathway for the initiation of blood coagulation is the tissue factor (extrinsic) pathway. The pathways are a series of reactions, in which a zymogen (inactive enzyme precursor) of a serine protease and its glycoprotein co-factor are activated to become active components that then catalyze the next reaction in the cascade, ultimately resulting in cross-linked fibrin. Coagulation factors are generally indicated by Roman numerals, with a lowercase a appended to indicate an active form.

The coagulation factors are generally serine proteases (enzymes), which act by cleaving downstream proteins. The exceptions are tissue factor, FV, FVIII, FXIII. Tissue factor, FV and FVIII are glycoproteins, and Factor XIII is a transglutaminase. The coagulation factors circulate as inactive zymogens. The coagulation cascade is therefore classically divided into three pathways. The tissue factor and contact activation pathways both activate the "final common pathway" of factor X, thrombin and fibrin.

Tissue factor pathway (extrinsic)

The main role of the tissue factor pathway is to generate a "thrombin burst", a process by which thrombin, the most important constituent of the coagulation cascade in terms of its feedback activation roles, is released very rapidly. FVIIa circulates in a higher amount than any other activated coagulation factor. The process includes the following steps:

1. Following damage to the blood vessel, FVII leaves the circulation and comes into contact with tissue factor (TF) expressed on tissue-factor-bearing cells (stromal fibroblasts and leukocytes), forming an activated complex (TF-FVIIa).
2. TF-FVIIa activates FIX and FX.
3. FVII is itself activated by thrombin, FXIa, FXII and FXa.
4. The activation of FX (to form FXa) by TF-FVIIa is almost immediately inhibited by tissue factor pathway inhibitor (TFPI).
5. FXa and its co-factor FVa form the prothrombinase complex, which activates prothrombin to thrombin.
6. Thrombin then activates other components of the coagulation cascade, including FV and FVIII (which forms a complex with FIX), and activates and releases FVIII from being bound to vWF.
7. FVIIIa is the co-factor of FIXa, and together they form the "tenase" complex, which activates FX; and so the cycle continues. ("Tenase" is a contraction of "ten" and the suffix "-ase" used for enzymes.)

Contact activation pathway (intrinsic)

The contact activation pathway begins with formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK), prekallikrein, and FXII (Hageman factor). Prekallikrein is converted to kallikrein and FXII becomes FXIIa. FXIIa converts FXI into FXIa. Factor XIa activates FIX, which with its co-factor FVIIIa form the tenase complex, which activates FX to FXa. The minor role that the contact activation pathway has in initiating clot formation can be illustrated by the fact that patients with severe deficiencies of FXII, HMWK, and prekallikrein do not have a bleeding disorder. Instead, contact activation system seems to be more involved in inflammation, and innate immunity. Despite this, interference with the pathway may confer protection against thrombosis without a significant bleeding risk.

Final common pathway

The division of coagulation in two pathways is arbitrary, originating from laboratory tests in which clotting times were measured either after the clotting was initiated by glass, the intrinsic pathway; or clotting was initiated by thromboplastin (a mix of tissue factor and phospholipids), the extrinsic pathway.

Further, the final common pathway scheme implies that prothrombin is converted to thrombin only when acted upon by the intrinsic or extrinsic pathways, which is an oversimplification. In fact, thrombin is generated by activated platelets at the initiation of the platelet plug, which in turn promotes more platelet activation.

Thrombin functions not only to convert fibrinogen to fibrin, it also activates Factors VIII and V and their inhibitor protein C (in the presence of thrombomodulin); and it activates Factor XIII, which forms covalent bonds that crosslink the fibrin polymers that form from activated monomers.

The coagulation cascade is maintained in a prothrombotic state by the continued activation of FVIII and FIX to form the tenase complex until it is down-regulated by the anticoagulant pathways.

Cell-based scheme of coagulation

A newer model of coagulation mechanism explains the intricate combination of cellular and biochemical events that occur during the coagulation process in vivo. Along with the procoagulant and anticoagulant plasma proteins, normal physiologic coagulation requires the presence of two cell types for formation of coagulation complexes: cells that express tissue factor (usually extravascular) and platelets.

The coagulation process occurs in two phases. First is the initiation phase, which occurs in tissue-factor-expressing cells. This is followed by the propagation phase, which occurs on activated platelets. The initiation phase, mediated by the tissue factor exposure, proceeds via the classic extrinsic pathway and contributes to about 5% of thrombin production. The amplified production of thrombin occurs via the classic intrinsic pathway in the propagation phase; about 95% of thrombin generated will be during this second phase.

Cofactors

Various substances are required for the proper functioning of the coagulation cascade:

Calcium and phospholipid

Calcium and phospholipid (a platelet membrane constituent) are required for the tenase and prothrombinase complexes to function. Calcium mediates the binding of the complexes via the terminal gamma-carboxy residues on FXa and FIXa to the phospholipid surfaces expressed by platelets, as well as procoagulant microparticles or microvesicles shed from them. Calcium is also required at other points in the coagulation cascade.

Vitamin K

Vitamin K is an essential factor to a hepatic gamma-glutamyl carboxylase that adds a carboxyl group to glutamic acid residues on factors II, VII, IX and X, as well as Protein S, Protein C and Protein Z. In adding the gamma-carboxyl group to glutamate residues on the immature clotting factors, Vitamin K is itself oxidized. Another enzyme, Vitamin K epoxide reductase (VKORC), reduces vitamin K back to its active form. Vitamin K epoxide reductase is pharmacologically important as a target of anticoagulant drugs warfarin and related coumarins such as acenocoumarol, phenprocoumon, and dicumarol. These drugs create a deficiency of reduced vitamin K by blocking VKORC, thereby inhibiting maturation of clotting factors. Vitamin K deficiency from other causes (e.g., in malabsorption) or impaired vitamin K metabolism in disease (e.g., in liver failure) lead to the formation of PIVKAs (proteins formed in vitamin K absence), which are partially or totally non-gamma carboxylated, affecting the coagulation factors' ability to bind to phospholipid.

Regulators

Coagulation with arrows for negative and positive feedback.

 

Five mechanisms keep platelet activation and the coagulation cascade in check. Abnormalities can lead to an increased tendency toward thrombosis:

Protein C

Protein C is a major physiological anticoagulant. It is a vitamin K-dependent serine protease enzyme that is activated by thrombin into activated protein C (APC). Protein C is activated in a sequence that starts with Protein C and thrombin binding to a cell surface protein thrombomodulin. Thrombomodulin binds these proteins in such a way that it activates Protein C. The activated form, along with protein S and a phospholipid as cofactors, degrades FVa and FVIIIa. Quantitative or qualitative deficiency of either (protein C or protein S) may lead to thrombophilia (a tendency to develop thrombosis). Impaired action of Protein C (activated Protein C resistance), for example by having the "Leiden" variant of Factor V or high levels of FVIII, also may lead to a thrombotic tendency.

Antithrombin

Antithrombin is a serine protease inhibitor (serpin) that degrades the serine proteases: thrombin, FIXa, FXa, FXIa, and FXIIa. It is constantly active, but its adhesion to these factors is increased by the presence of heparan sulfate (a glycosaminoglycan) or the administration of heparins (different heparinoids increase affinity to FXa, thrombin, or both). Quantitative or qualitative deficiency of antithrombin (inborn or acquired, e.g., in proteinuria) leads to thrombophilia.

Tissue factor pathway inhibitor (TFPI)

Tissue factor pathway inhibitor (TFPI) limits the action of tissue factor (TF). It also inhibits excessive TF-mediated activation of FVII and FX.

Plasmin

Plasmin is generated by proteolytic cleavage of plasminogen, a plasma protein synthesized in the liver. This cleavage is catalyzed by tissue plasminogen activator (t-PA), which is synthesized and secreted by endothelium. Plasmin proteolytically cleaves fibrin into fibrin degradation products that inhibit excessive fibrin formation.

Prostacyclin

Prostacyclin (PGI₂) is released by endothelium and activates platelet G_s protein-linked receptors. This, in turn, activates adenylyl cyclase, which synthesizes cAMP. cAMP inhibits platelet activation by decreasing cytosolic levels of calcium and, by doing so, inhibits the release of granules that would lead to activation of additional platelets and the coagulation cascade.

Fibrinolysis

Eventually, blood clots are reorganised and resorbed by a process termed fibrinolysis. The main enzyme responsible for this process (plasmin) is regulated by various activators and inhibitors.

Role in immune system

The coagulation system overlaps with the immune system. Coagulation can physically trap invading microbes in blood clots. Also, some products of the coagulation system can contribute to the innate immune system by their ability to increase vascular permeability and act as chemotactic agents for phagocytic cells. In addition, some of the products of the coagulation system are directly antimicrobial. For example, beta-lysine, an amino acid produced by platelets during coagulation, can cause lysis of many Gram-positive bacteria by acting as a cationic detergent. Many acute-phase proteins of inflammation are involved in the coagulation system. In addition, pathogenic bacteria may secrete agents that alter the coagulation system, e.g. coagulase and streptokinase.

Assessment

Numerous tests are used to assess the function of the coagulation system:

• Common: aPTT, PT (also used to determine INR), fibrinogen testing (often by the Clauss method), platelet count, platelet function testing (often by PFA-100), thrombodynamics test.
• Other: TCT, bleeding time, mixing test (whether an abnormality corrects if the patient's plasma is mixed with normal plasma), coagulation factor assays, antiphospholipid antibodies, D-dimer, genetic tests (e.g. factor V Leiden, prothrombin mutation G20210A), dilute Russell's viper venom time (dRVVT), miscellaneous platelet function tests, thromboelastography (TEG or Sonoclot), euglobulin lysis time (ELT).

The contact activation (intrinsic) pathway is initiated by activation of the "contact factors" of plasma, and can be measured by the activated partial thromboplastin time (aPTT) test. 

The tissue factor (extrinsic) pathway is initiated by release of tissue factor (a specific cellular lipoprotein), and can be measured by the prothrombin time (PT) test. PT results are often reported as ratio (INR value) to monitor dosing of oral anticoagulants such as warfarin. 

The quantitative and qualitative screening of fibrinogen is measured by the thrombin clotting time (TCT). Measurement of the exact amount of fibrinogen present in the blood is generally done using the Clauss method for fibrinogen testing. Many analysers are capable of measuring a "derived fibrinogen" level from the graph of the Prothrombin time clot.

If a coagulation factor is part of the contact activation or tissue factor pathway, a deficiency of that factor will affect only one of the tests: Thus hemophilia A, a deficiency of factor VIII, which is part of the contact activation pathway, results in an abnormally prolonged aPTT test but a normal PT test. The exceptions are prothrombin, fibrinogen, and some variants of FX that can be detected only by either aPTT or PT. If an abnormal PT or aPTT is present, additional testing will occur to determine which (if any) factor is present as aberrant concentrations.

Deficiencies of fibrinogen (quantitative or qualitative) will affect all screening tests.

Role in disease

Coagulation defects may cause hemorrhage or thrombosis, and occasionally both, depending on the nature of the defect.

The GP1b-IX receptor complex. This protein receptor complex is found on the surface of platelets, and in conjunction with GPV allows for platelets to adhere to the site of injury. Mutations in the genes associated with the glycoprotein Ib-IX-V complex are characteristic of Bernard–Soulier syndrome

Platelet disorders

Platelet disorders are either congenital or acquired. Examples of congenital platelet disorders are Glanzmann's thrombasthenia, Bernard–Soulier syndrome (abnormal glycoprotein Ib-IX-V complex), gray platelet syndrome (deficient alpha granules), and delta storage pool deficiency (deficient dense granules). Most are rare. They predispose to hemorrhage. Von Willebrand disease is due to deficiency or abnormal function of von Willebrand factor, and leads to a similar bleeding pattern; its milder forms are relatively common.

Decreased platelet numbers (thrombocytopenia) is due to insufficient production (e.g., myelodysplastic syndrome or other bone marrow disorders), destruction by the immune system (immune thrombocytopenic purpura/ITP), or consumption (e.g., thrombotic thrombocytopenic purpura/TTP, hemolytic-uremic syndrome/HUS, paroxysmal nocturnal hemoglobinuria/PNH, disseminated intravascular coagulation/DIC, heparin-induced thrombocytopenia/HIT). Most consumptive conditions lead to platelet activation, and some are associated with thrombosis.

Coagulation factor disorders

The best-known coagulation factor disorders are the hemophilias. The three main forms are hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency or "Christmas disease") and hemophilia C (factor XI deficiency, mild bleeding tendency). Hemophilia A and B are X-linked recessive disorders, whereas Hemophilia C is a much more rare autosomal recessive disorder most commonly seen in Ashkenazi Jews.

Von Willebrand disease (which behaves more like a platelet disorder except in severe cases), is the most common hereditary bleeding disorder and is characterized as being inherited autosomal recessive or dominant. In this disease, there is a defect in von Willebrand factor (vWF), which mediates the binding of glycoprotein Ib (GPIb) to collagen. This binding helps mediate the activation of platelets and formation of primary hemostasis.

Bernard–Soulier syndrome is a defect or deficiency in GPIb. GPIb, the receptor for vWF, can be defective and lead to lack of primary clot formation (primary hemostasis) and increased bleeding tendency. This is an autosomal recessive inherited disorder.

Thrombasthenia of Glanzmann and Naegeli (Glanzmann thrombasthenia) is extremely rare. It is characterized by a defect in GPIIb/IIIa fibrinogen receptor complex. When GPIIb/IIIa receptor is dysfunctional, fibrinogen cannot cross-link platelets, which inhibits primary hemostasis. This is an autosomal recessive inherited disorder.

In liver failure (acute and chronic forms), there is insufficient production of coagulation factors by the liver; this may increase bleeding risk. 

Deficiency of Vitamin K may also contribute to bleeding disorders because clotting factor maturation depends on Vitamin K. 

Thrombosis is the pathological development of blood clots. These clots may break free and become mobile, forming an embolus or grow to such a size that occludes the vessel in which it developed. An embolism is said to occur when the thrombus (blood clot) becomes a mobile embolus and migrates to another part of the body, interfering with blood circulation and hence impairing organ function downstream of the occlusion. This causes ischemia and often leads to ischemic necrosis of tissue. Most cases of venous thrombosis are due to acquired states (older age, surgery, cancer, immobility) or inherited thrombophilias (e.g., antiphospholipid syndrome, factor V Leiden, and various other genetic deficiencies or variants).

Mutations in factor XII have been associated with an asymptomatic prolongation in the clotting time and possibly a tendency toward thrombophlebitis. Other mutations have been linked with a rare form of hereditary angioedema (type III) essentialism.

Pharmacology

Procoagulants

The use of adsorbent chemicals, such as zeolites, and other hemostatic agents are also used for sealing severe injuries quickly (such as in traumatic bleeding secondary to gunshot wounds). Thrombin and fibrin glue are used surgically to treat bleeding and to thrombose aneurysms.

Desmopressin is used to improve platelet function by activating arginine vasopressin receptor 1A. 

Coagulation factor concentrates are used to treat hemophilia, to reverse the effects of anticoagulants, and to treat bleeding in patients with impaired coagulation factor synthesis or increased consumption. Prothrombin complex concentrate, cryoprecipitate and fresh frozen plasma are commonly used coagulation factor products. Recombinant activated human factor VII is increasingly popular in the treatment of major bleeding.

Tranexamic acid and aminocaproic acid inhibit fibrinolysis and lead to a de facto reduced bleeding rate. Before its withdrawal, aprotinin was used in some forms of major surgery to decrease bleeding risk and need for blood products.

Rivaroxaban drug bound to the coagulation factor Xa. The drug prevents this protein from activating the coagulation pathway by inhibiting its enzymatic activity.

Anticoagulants

Anticoagulants and anti-platelet agents are amongst the most commonly used medications. Anti-platelet agents include aspirin, dipyridamole, ticlopidine, clopidogrel, ticagrelor and prasugrel; the parenteral glycoprotein IIb/IIIa inhibitors are used during angioplasty. Of the anticoagulants, warfarin (and related coumarins) and heparin are the most commonly used. Warfarin affects the vitamin K-dependent clotting factors (II, VII, IX, X) and protein C and protein S, whereas heparin and related compounds increase the action of antithrombin on thrombin and factor Xa. A newer class of drugs, the direct thrombin inhibitors, is under development; some members are already in clinical use (such as lepirudin). Also in clinical use are other small molecular compounds that interfere directly with the enzymatic action of particular coagulation factors (the directly acting oral anticoagulants: dabigatran, rivaroxaban, apixaban, and edoxaban).

Grigori Rasputin

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Grigori_Rasputin 

Grigori Rasputin
Native name	Григорий Ефимович Распутин
Church	Russian Orthodox Church
Personal details
Birth name	Grigori Yefimovich Rasputin
Born	21 January [O.S. 9 January] 1869 Pokrovskoye, Tyumensky Uyezd, Tobolsk Governorate (Siberia), Russian Empire
Died	30 December [O.S. 17 December] 1916 (aged 47) Saint Petersburg, Russian Empire
Nationality	Russian
Parents	Yefim Rasputin Anna Parshukova
Spouse	Praskovya Fedorovna Dubrovina (m. 1887)
Children	Dmitri (1895–1937) Maria (1898–1977) Varvara (1900–1925)

Grigori Yefimovich Rasputin (/ræˈspjuːtɪn/; Russian: Григорий Ефимович Распутин [ɡrʲɪˈɡorʲɪj jɪˈfʲiməvʲɪtɕ rɐˈsputʲɪn]; 21 January [O.S. 9 January] 1869 – 30 December [O.S. 17 December] 1916) was a Russian mystic and self-proclaimed holy man who befriended the family of Emperor Nicholas II, the last monarch of Russia, and gained considerable influence in late imperial Russia.

Rasputin was born to a peasant family in the Siberian village of Pokrovskoye in the Tyumensky Uyezd of Tobolsk Governorate (now Yarkovsky District of Tyumen Oblast). He had a religious conversion experience after taking a pilgrimage to a monastery in 1897. He has been described as a monk or as a "strannik" (wanderer or pilgrim), though he held no official position in the Russian Orthodox Church. He traveled to St. Petersburg in 1903 or the winter of 1904–05, where he captivated some church and social leaders. He became a society figure and met the tsar and Tsarina Alexandra in November 1905.

In late 1906, Rasputin began acting as a healer for the only son of Tsar Nicholas II, Alexei, who suffered from hemophilia. He was a divisive figure at court, seen by some Russians as a mystic, visionary, and prophet, and by others as a religious charlatan. The high point of Rasputin's power was in 1915 when Nicholas II left St. Petersburg to oversee Russian armies fighting World War I, increasing both Alexandra and Rasputin's influence. Russian defeats mounted during the war, however, and both Rasputin and Alexandra became increasingly unpopular. In the early morning of 30 December [O.S. 17 December] 1916, Rasputin was assassinated by a group of conservative noblemen who opposed his influence over Alexandra and the tsar.

Historians often suggest that Rasputin's terrible reputation helped discredit the tsarist government and thus helped precipitate the overthrow of the Romanov dynasty which happened a few weeks after he was assassinated. Accounts of his life and influence were often based on hearsay and rumor.

Early life

Pokrovskoye in 1912

 

Rasputin with his children

Rasputin was born a peasant in the small village of Pokrovskoye, along the Tura River in the Tobolsk Governorate (now Tyumen Oblast) in Siberia. According to official records, he was born on 21 January [O.S. 9 January] 1869 and christened the following day. He was named for St. Gregory of Nyssa, whose feast was celebrated on 10 January.

There are few records of Rasputin's parents. His father, Yefim, was a peasant farmer and church elder who had been born in Pokrovskoye in 1842, and married Rasputin's mother, Anna Parshukova, in 1863. Yefim also worked as a government courier, ferrying people and goods between Tobolsk and Tyumen The couple had seven other children, all of whom died in infancy and early childhood; there may have been a ninth child, Feodosiya. According to historian Joseph T. Fuhrmann, Rasputin was certainly close to Feodosiya and was godfather to her children, but "the records that have survived do not permit us to say more than that".

According to historian Douglas Smith, Rasputin's youth and early adulthood are "a black hole about which we know almost nothing", though the lack of reliable sources and information did not stop others from fabricating stories about his parents and his youth after Rasputin's rise to fame. Historians agree, however, that like most Siberian peasants, including his mother and father, Rasputin was not formally educated and remained illiterate well into his early adulthood. Local archival records suggest that he had a somewhat unruly youth – possibly involving drinking, small thefts, and disrespect for local authorities – but contain no evidence of his being charged with stealing horses, blasphemy, or bearing false witness, all major crimes that he was later rumored to have committed as a young man.

In 1886, Rasputin travelled to Abalak, Russia, some 250 km east-northeast of Tyumen and 2,800 km east of Moscow, where he met a peasant girl named Praskovya Dubrovina. After a courtship of several months, they married in February 1887. Praskovya remained in Pokrovskoye throughout Rasputin's later travels and rise to prominence and remained devoted to him until his death. The couple had seven children, though only three survived to adulthood: Dmitry (b. 1895), Maria (b. 1898), and Varvara (b. 1900).

Religious conversion

In 1897, Rasputin developed a renewed interest in religion and left Pokrovskoye to go on a pilgrimage. His reasons for doing so are unclear; according to some sources, Rasputin left the village to escape punishment for his role in a horse theft. Other sources suggest that he had a vision – either of the Virgin Mary or of St. Simeon of Verkhoturye – while still others suggest that Rasputin's pilgrimage was inspired by his interactions with a young theological student, Melity Zaborovsky. Whatever his reasons, Rasputin's departure was a radical life change: he was twenty-eight, had been married ten years, and had an infant son with another child on the way. According to Douglas Smith, his decision "could only have been occasioned by some sort of emotional or spiritual crisis".

Rasputin had undertaken earlier, shorter pilgrimages to the Holy Znamensky Monastery at Abalak and to Tobolsk's cathedral, but his visit to the St. Nicholas Monastery at Verkhoturye in 1897 was transformative. There, he met and was "profoundly humbled" by a starets (elder) known as Makary. Rasputin may have spent several months at Verkhoturye, and it was perhaps here that he learned to read and write, but he later complained about the monastery, claiming that some of the monks engaged in homosexuality and criticizing monastic life as too coercive. He returned to Pokrovskoye a changed man, looking disheveled and behaving differently than he had before. He became a vegetarian, swore off alcohol, and prayed and sang much more fervently than he had in the past.

Rasputin spent the years that followed living as a Strannik (a holy wanderer, or pilgrim), leaving Pokrovskoye for months or even years at a time to wander the country and visited a variety of holy sites. It is possible that Rasputin wandered as far as Athos, Greece – the center of Eastern Orthodox monastic life – in 1900.

By the early 1900s, Rasputin had developed a small circle of acolytes, primarily family members and other local peasants, who prayed with him on Sundays and other holy days when he was in Pokrovskoye. Building a makeshift chapel in Efim's root cellar – Rasputin was still living within his father's household at the time – the group held secret prayer meetings there. These meetings were the subject of some suspicion and hostility from the village priest and other villagers. It was rumored that female followers were ceremonially washing him before each meeting, that the group sang strange songs that the villagers had not heard before, and even that Rasputin had joined the Khlysty, a religious sect whose ecstatic rituals were rumored to include self-flagellation and sexual orgies. According to historian Joseph Fuhrmann, however, "repeated investigations failed to establish that Rasputin was ever a member of the sect", and rumors that he was a Khlyst appear to have been unfounded.

Rise to prominence

Makary, Bishop Theofan (Feofan) of Poltava and Rasputin

Word of Rasputin's activity and charisma began to spread in Siberia during the early 1900s. Sometime between 1902 and 1904, he travelled to the city of Kazan on the Volga river, where he acquired a reputation as a wise and perceptive starets, or holy man, who could help people resolve their spiritual crises and anxieties. Despite rumors that Rasputin was having sex with some of his female followers, he won over the father superior of the Seven Lakes Monastery outside Kazan, as well as a local church officials Archimandrite Andrei and Bishop Chrysthanos, who gave him a letter of recommendation to Bishop Sergei, the rector of the St. Petersburg Theological Seminary at the Alexander Nevsky Monastery, and arranged for him to travel to St. Petersburg, either in 1903 or in the winter of 1904–05.

Upon meeting Sergei at the Nevsky Monastery, Rasputin was introduced to church leaders, including Archimandrite Feofan, who was the inspector of the theological seminary, was well-connected in St. Petersburg society, and later served as confessor to the tsar and his wife. Feofan was so impressed with Rasputin that he invited him to stay in his home and became one of Rasputin's most important and influential friends in St. Petersburg.

According to Joseph T. Fuhrmann, Rasputin stayed in St. Petersburg for only a few months on his first visit and returned to Pokrovskoye in the fall of 1903. Historian Douglas Smith, however, argues that it is impossible to know whether Rasputin stayed in St. Petersburg or returned to Pokrovskoye at some point between his first arrival there and 1905. Regardless, by 1905 Rasputin had formed friendships with several members of the aristocracy, including the "Black Princesses", Militsa and Anastasia of Montenegro, who had married the tsar's cousins (Grand Duke Peter Nikolaevich and Grand Duke Nikolai Nikolaevich), and were instrumental in introducing Rasputin to the tsar and his family.

Rasputin first met the tsar on 1 November 1905, at the Peterhof Palace. The tsar recorded the event in his diary, writing that he and Alexandra had "made the acquaintance of a man of God – Grigory, from Tobolsk province". Rasputin returned to Pokrovskoye shortly after their first meeting and did not return to St. Petersburg until July 1906. On his return, Rasputin sent Nicholas a telegram asking to present the tsar with an icon of Simeon of Verkhoturye. He met with Nicholas and Alexandra on 18 July and again in October, when he first met their children. At some point, the royal family became convinced that Rasputin possessed the power to heal Alexei, but historians disagree over when: according to Orlando Figes, Rasputin was first introduced to the tsar and tsarina as a healer who could help their son in November 1905, while Joseph Fuhrmann has speculated that it was in October 1906 that Rasputin was first asked to pray for the health of Alexei.

Healer to Alexei

Alexandra Feodorovna with her children, Rasputin and the nurse Maria Ivanova Vishnyakova (1908)

 

Much of Rasputin's influence with the royal family stemmed from the belief by Alexandra and others that he had eased the pain and stopped the bleeding of the tsarevich – who suffered from hemophilia – on several occasions. According to historian Marc Ferro, the tsarina had a "passionate attachment" to Rasputin as a result of her belief that he could heal her son's affliction. Harold Shukman wrote that Rasputin became "an indispensable member of the royal entourage" as a result. It is unclear when Rasputin first learned of Alexei's hemophilia, or when he first acted as a healer for Alexei. He may have been aware of Alexei's condition as early as October 1906, and was summoned by Alexandra to pray for Alexei when he had an internal hemorrhage in the spring of 1907. Alexei recovered the next morning. Rasputin had been rumored to be capable of faith-healing since his arrival in St. Petersburg, and the tsarina's friend Anna Vyrubova became convinced that Rasputin had miraculous powers shortly thereafter. Vyrubova would become one of Rasputin's most influential advocates.

During the summer of 1912, Alexei developed a hemorrhage in his thigh and groin after a jolting carriage ride near the royal hunting grounds at Spala, which caused a large hematoma. In severe pain and delirious with fever, the tsarevich appeared to be close to death. In desperation, the tsarina asked Vyrubova to send Rasputin (who was in Siberia) a telegram, asking him to pray for Alexei. Rasputin wrote back quickly, telling the tsarina that "God has seen your tears and heard your prayers. Do not grieve. The Little One will not die. Do not allow the doctors to bother him too much." The next morning, Alexei's condition was unchanged, but Alexandra was encouraged by the message and regained some hope that Alexei would survive. Alexei's bleeding stopped the following day.

Historian Robert K. Massie has calls Alexei's recovery "one of the most mysterious episodes of the whole Rasputin legend". The cause of his recovery is unclear: Massie speculated that Rasputin's suggestion not to let doctors disturb Alexei had aided his recovery by allowing him to rest and heal, or that his message may have aided Alexei's recovery by calming Alexandra and reducing the emotional stress on Alexei. Alexandra, however, believed that Rasputin had performed a miracle, and concluded that he was essential to Alexei's survival. Some writers and historians, such as Ferro, claim that Rasputin stopped Alexei's bleeding on other occasions through hypnosis.

Controversy

Rasputin among admirers, 1914

The royal family's belief that Rasputin possessed the power to heal Alexei brought him considerable status and power at court. The tsar appointed Rasputin his lampadnik (lamplighter) who was charged with keeping the lamps lit that burned in front of religious icons in the palace, and he thus had regular access to the palace and royal family. By December 1906, Rasputin had become close enough to the royal family to ask a special favor of the tsar: that he be permitted to change his surname to Rasputin-Novyi (Rasputin-New). Nicholas granted the request and the name change was speedily processed, suggesting that the tsar viewed and treated Rasputin favorably at that time. Rasputin used his status and power to full effect, accepting bribes and sexual favors from admirers and working diligently to expand his influence. He soon became a controversial figure; he was accused by his enemies of religious heresy and rape, was suspected of exerting undue political influence over the tsar, and was even rumored to be having an affair with the tsarina.

Alternative religious movements had become popular among the city's aristocracy before Rasputin's arrival in St. Petersburg in 1903, such as spiritualism and theosophy, and many of the aristocracy were intensely curious about the occult and the supernatural. The Saint Petersburg elite were fascinated by Rasputin but did not widely accept him. He did not fit in with the royal family, and he had a very strained relationship with the Russian Orthodox Church. The Holy Synod frequently attacked Rasputin, accusing him of a variety of immoral or evil practices.

Rasputin with his wife and daughter Matryona (Maria) in his St. Petersburg apartment in 1911

 

Caricature of Rasputin and the Imperial couple (1916)

 

World War I, the disappearance of feudalism, and a meddling government bureaucracy all contributed to Russia's declining economy at a very rapid rate. Many laid the blame with Alexandra and with Rasputin, because of his influence over her. Here is an example:

Vladimir Purishkevich was an outspoken member of the Duma. On 19 November 1916, Purishkevich made a rousing speech in the Duma, in which he stated, "The tsar's ministers who have been turned into marionettes, marionettes whose threads have been taken firmly in hand by Rasputin and the Empress Alexandra Fyodorovna – the evil genius of Russia and the Tsarina… who has remained a German on the Russian throne and alien to the country and its people." Felix Yusupov attended the speech and afterwards contacted Purishkevich, who quickly agreed to participate in the murder of Rasputin.

Rasputin's influence over the royal family was used against him and the Romanovs by politicians and journalists who wanted to weaken the integrity of the dynasty, force the tsar to give up his absolute political power, and separate the Russian Orthodox Church from the state.

Assassination attempt

On 12 July [O.S. 29 June] 1914 a 33-year-old peasant woman named Chionya Guseva attempted to assassinate Rasputin by stabbing him in the stomach outside his home in Pokrovskoye. Rasputin was seriously wounded, and for a time it was not clear that he would survive. After surgery and some time in a hospital in Tyumen, he recovered.

Guseva was a follower of Iliodor, a former priest who had supported Rasputin before denouncing his sexual escapades and self-aggrandizement in December 1911. A radical conservative and anti-semite, Iliodor had been part of a group of establishment figures who had attempted to drive a wedge between the royal family and Rasputin in 1911. When this effort failed, Iliodor was banished from Saint Petersburg and was ultimately defrocked. Guseva claimed to have acted alone, having read about Rasputin in the newspapers and believing him to be a "false prophet and even an Antichrist". Both the police and Rasputin, however, believed that Iliodor had played some role in the attempt on Rasputin's life. Iliodor fled the country before he could be questioned about the assassination attempt, and Guseva was found to be not responsible for her actions by reason of insanity.

Death

Felix Yusupov (1914) married Irina Aleksandrovna Romanova, the Tsar's niece.

A group of nobles led by Prince Felix Yusupov, Grand Duke Dmitri Pavlovich, and right-wing politician Vladimir Purishkevich decided that Rasputin's influence over the tsarina had made him a threat to the empire, and they concocted a plan in December 1916 to kill him, apparently by luring him to the Yusupovs' Moika Palace.

Basement of the Yusupov Palace on the Moika in St. Petersburg where Rasputin was murdered

 

 

The wooden Bolshoy Petrovsky Bridge, from which Rasputin's body was thrown into the Malaya Nevka River

 

Rasputin was murdered during the early morning on 30 December [O.S. 17 December] 1916 at the home of Felix Yusupov. He died of three gunshot wounds, one of which was a close-range shot to his forehead. Little is certain about his death beyond this, and the circumstances of his death have been the subject of considerable speculation. According to historian Douglas Smith, "what really happened at the Yusupov home on 17 December will never be known". The story that Yusupov recounted in his memoirs, however, has become the most frequently told version of events.

Rasputin's body with bullet wound in forehead

 

Yusupov claimed that he invited Rasputin to his home shortly after midnight and ushered him into the basement. Yusupov offered Rasputin tea and cakes which had been laced with cyanide. Rasputin initially refused the cakes but then began to eat them and, to Yusupov's surprise, he did not appear to be affected by the poison. Rasputin then asked for some Madeira wine (which had also been poisoned) and drank three glasses, but still showed no sign of distress. At around 2:30 am, Yusupov excused himself to go upstairs, where his fellow conspirators were waiting. He took a revolver from Dmitry Pavlovich, then returned to the basement and told Rasputin that he'd "better look at the crucifix and say a prayer", referring to a crucifix in the room, then shot him once in the chest. The conspirators then drove to Rasputin's apartment, with Sukhotin wearing Rasputin's coat and hat in an attempt to make it look as though Rasputin had returned home that night. They then returned to the Moika Palace and Yusupov went back to the basement to ensure that Rasputin was dead. Suddenly, Rasputin leapt up and attacked Yusupov, who freed himself with some effort and fled upstairs. Rasputin followed and made it into the palace's courtyard before being shot by Purishkevich and collapsing into a snowbank. The conspirators then wrapped his body in cloth, drove it to the Petrovsky Bridge, and dropped it into the Malaya Nevka River.

Aftermath

News of Rasputin's murder spread quickly, even before his body was found. According to Douglas Smith, Purishkevich spoke openly about Rasputin's murder to two soldiers and to a policeman who was investigating reports of shots shortly after the event, but he urged them not to tell anyone else. An investigation was launched the next morning. The Stock Exchange Gazette ran a report of Rasputin's death "after a party in one of the most aristocratic homes in the center of the city" on the afternoon of 30 December [O.S. 17 December] 1916.

Two workmen noticed blood on the railing of the Petrovsky Bridge and found a boot on the ice below, and police began searching the area. Rasputin's body was found under the river ice on 1 January (O.S. 19 December) approximately 200 meters downstream from the bridge. Dr. Dmitry Kosorotov, the city's senior autopsy surgeon, conducted an autopsy. Kosorotov's report was lost, but he later stated that Rasputin's body had shown signs of severe trauma, including three gunshot wounds (one at close range to the forehead), a slice wound to his left side, and many other injuries, many of which Kosorotov felt had been sustained post-mortem. Kosorotov found a single bullet in Rasputin's body but stated that it was too badly deformed and of a type too widely used to trace. He found no evidence that Rasputin had been poisoned. According to both Douglas Smith and Joseph Fuhrmann, Kosorotov found no water in Rasputin's lungs, and reports were incorrect that Rasputin had been thrown into the water alive. Some later accounts claimed that Rasputin's penis had been severed, but Kosorotov found his genitals intact.

Rasputin was buried on 2 January (O.S. 21 December) at a small church that Anna Vyrubova had been building at Tsarskoye Selo. The funeral was attended only by the royal family and a few of their intimates. Rasputin's wife, mistress, and children were not invited, although his daughters met with the royal family at Vyrubova's home later that day. His body was exhumed and burned by a detachment of soldiers shortly after the tsar abdicated the throne in March 1917, in order to prevent his burial site from becoming a rallying point for supporters of the old regime.

Theory of British involvement

Some writers have suggested that agents of the British Secret Intelligence Service (BSIS) were involved in Rasputin's assassination. According to this theory, British agents were concerned that Rasputin was urging the tsar to make a separate peace with Germany, which would allow Germany to concentrate its military efforts on the Western Front. There are several variants of this theory, but they generally suggest that British intelligence agents were directly involved in planning and carrying out the assassination under the command of Samuel Hoare and Oswald Rayner, who had attended Oxford University with Yusopov, or that Rayner had personally shot Rasputin. However, historians do not seriously consider this theory. According to historian Douglas Smith, "there is no convincing evidence that places any British agents at the murder scene". Historian Keith Jeffery states that if British Intelligence agents had been involved in the assassination of Rasputin, "I would have expected to find some trace of that" in the Secret Intelligence Service archives, but no such evidence exists.

Daughter

Rasputin's daughter, Maria Rasputin (born Matryona Rasputina) (1898–1977), emigrated to France after the October Revolution and then to the United States. There, she worked as a dancer and then a lion tamer in a circus.