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Vladimir Purishkevich

Vladimir Mitrofanovich Purishkevich (Владимир Митрофанович Пуришкевич, ; 24 August 1870 – 1 February 1920) was a Russian politician and right-wing extremist known for his monarchist, ultra-nationalist, antisemitic and anticommunist views. He helped lead the paramilitary Black Hundreds during the Russian Revolution of 1905. He later served in the State Duma, where he gained a reputation for courting of public controversy. Together with Felix Yusupov and Dmitri Pavlovich he took part in the assassination of Grigori Rasputin in late 1916.

After the February Revolution, Purishkevich was one of the only leaders of the Black Hundreds to remain politically active. He eventually joined the White movement and died from typhus in 1920.

Early career
Born as the son of a poor nobleman in Kishinev, Bessarabia (now Moldova), Purishkevich graduated from Novorossiysk University with a degree in classical philology. Around 1900, he moved to Saint Petersburg. He became a member of the Russian Assembly group and was appointed under Vyacheslav von Plehve.

Purishkevich was a hardline supporter of Russification and sacerdotal autocracy. Purishkevich was hostile towards Jews, who he believed to be the "vanguard of the revolutionary movement". He wanted Jews to be deported to Kolyma. He believed that the "Kadets, socialists, the intelligentsia, the press and councils of university professors" were all under the control of Jews.

During the Russian Revolution of 1905, Purishkevich helped organise the Black Hundreds, a reactionary, monarchist and ultra-nationalist militia that carried out a number of raids (with unofficial government approval) against revolutionary groups as well as pogroms against Jews. After the October Manifesto created the State Duma, he was elected as a deputy for the Bessarabian and Kursk province. He became one of the founders of the Union of the Russian People and served as its deputy chairman until 1907, when he split to form the Union of the Archangel Michael. In the Duma, he gained fame and infamy for his flamboyant speeches and scandalous behaviour, such as speaking on International Workers' Day with a red carnation in his fly.

When the first Russian women's congress convened in 1908, Purishkevich sent a letter to several of the participants calling it "an assembly of whores". One of the recipients of the letter, Anna Filosofova, made the letter public and took Purishkevich to court; he was sentenced to one month in jail.

Criticism of Rasputin
During World War I, Purishkevich became critical of the performance of the government, although not of the tsar himself; he saw the rise of pro-Russian sentiment during the war as a popular expression of support for the tsar. Purishkevich was particularly critical of the roles of Empress Alexandra and her close advisor Grigori Rasputin. On 3 November 1916, Purishkevich went to Mogilev and talked with Tsar Nicolas II about Rasputin.

On 19 November, Purishkevich delivered a speech in the Duma that denounced Rasputin and the conduct of the government. He compared Rasputin with the "False Dmitri", and argued that Rasputin's influence over the tsarina had made him a threat to the empire. He stated that the monarchy was becoming discredited:

"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."

He concluded that "While Rasputin is alive, we cannot win".

Killing of Rasputin

Prince Felix Yusupov was impressed by Purishkevich's speech criticizing Rasputin. He visited Purishkevich, who quickly agreed to participate in the killing of Rasputin. Also, Grand Duke Dmitri Pavlovich joined the conspiracy. Purishkevich talked to Samuel Hoare, the head of the British Secret Intelligence Service in Petrograd.

On the evening of 16 December 1916, the conspirators gathered in the Moika Palace and eventually killed Rasputin.

A curious policeman on duty on the other side of the Moika had heard the shots, rang at the door, and was sent away. Half an hour later, another policeman arrived, and Purishkevich invited him into the palace. Purishkevich told him that he had shot Rasputin and asked him to keep it quiet for the sake of the tsar.

They had planned to burn Rasputin's possessions. Sukhotin put on Rasputin's fur coat, rubber boots, and gloves. He left with Dmitri and Dr. Lazovert in Purishkevich's car, which suggests that Rasputin had left the palace alive. Because Purishkevich's wife refused to burn the fur coat and the boots in her small fireplace in the ambulance train, the conspirators went back to the palace with the larger items.

Yusupov and Dmitri were placed under house arrest in the Sergei Palace. The tsarina had refused to meet them but said that they could explain to her what had happened in a letter. Purishkevich assisted them and left the city to the Romanian front at ten in the evening. Because of his popularity, Purishkevich was neither punished nor exiled.

Revolutionary Russia

During the February Revolution in 1917, many right-wingers were arrested but Purishkevich was tolerated by the government and so was "virtually the only former national Black Hundred leader to maintain an active political life in Russia after the tsar's downfall". However, the revolution meant that Purishkevich initially had to moderate his politics. He called for the abolition of the Soviets, who were, in turn, calling for the abolition of the Duma.

In August 1917, he wanted a military dictatorship; he was arrested over the Kornilov Affair but was released. Following the failure of the putsch, he collaborated with Fyodor Viktorovich Vinberg in forming an underground monarchist organisation. During the October Revolution, he organized the "Committee for the Motherland's Salvation". He was joined by a number of officers, military cadets, and others.

At the time, Purishkevich was living in the Hotel Russia at Moika 60. He had a false passport under the surname "Yevreinov". On 18 November 1917, Purishkevich was arrested by the Red Guards for his participation in a counterrevolutionary conspiracy after the discovery of a letter sent by him to General Aleksei Maksimovich Kaledin in which he urged the Cossack leader to come and restore order in Petrograd. He became the first person to be tried in the Smolny Institute by the first Revolutionary Tribunal. He was condemned to eleven months of 'public work' and four years of imprisonment with obligatory community service and won the admiration of his fellow prisoners in the Fortress of St Peter and St Paul by his courageous bearing. He was given an amnesty on May 1 after the mediation of Felix Dzerzhinsky and Nikolay Krestinsky, as he refrained from any political activity. In jail, he had written a poem describing the Treaty of Brest-Litovsk as 'The Trotsky Peace'.

White Russia
After his release, he moved to White Army-controlled Southern Russia. There, during the Russian Civil War he published the monarchist journal Blagovest and returned openly to his traditional political stance of support for the monarchy, a unified Russia, and opposition to the Jews. In some of the towns occupied by the Volunteer Army, he gave lectures in which he denounced the British policy towards Russia. In 1918, he formed a new political party, the People's State Party, and called for an "open fight against Jewry"; the party collapsed after his death.

Vladimir Purishkevich died from typhus that raged Novorossiysk in 1920, just before the final evacuation of Denikin's Army.

Reputation
Purishkevich was described by contemporary Russian politician Vladimir Kokovtsov as a charming, unstable man who could not stay a single minute in one place. In 1925, Soviet writer Liubosh described Purishkevich as the 'first' fascist. He was subsequently referred to as a "leader of early Russian fascism" by Semyon Reznik, who also claimed that Purishkevich participated in numerous pogroms and was a significant proponent of the blood libel against Jews.

title: Vladimir Purishkevich


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Tropomyosin

Tropomyosin is a two-stranded alpha-helical, coiled coil protein found in many animal and fungal cells. In animals, it is an important component of the muscular system which works in conjunction with troponin to regulate muscle contraction. It is present in smooth and striated muscle tissues, which can be found in various organs and body systems, including the heart, blood vessels, respiratory system, and digestive system. In fungi, tropomyosin is found in cell walls and helps maintain the structural integrity of cells.

Tropomyosin is found in other eukaryotes too, but not in plants. Overall, tropomyosin is an important protein that plays a vital role in the proper functioning of many different organisms.

Tropomyosin and the actin skeleton
All organisms contain organelles that provide physical integrity to their cells. These type of organelles are collectively known as the cytoskeleton, and one of the most ancient systems is based on filamentous polymers of the protein actin. A polymer of a second protein, tropomyosin, is an integral part of most actin filaments in animals.

Tropomyosins are a large family of integral components of actin filaments that play a critical role in regulating the function of actin filaments in both muscle and nonmuscle cells. These proteins consist of rod-shaped coiled-coil hetero- or homo-dimers that lie along the α-helical groove of most actin filaments. Interaction occurs along the length of the actin filament, with dimers aligning in a head-to-tail fashion.

Tropomyosins are often categorised into two groups: muscle tropomyosin isoforms and nonmuscle tropomyosin isoforms. Muscle tropomyosin isoforms are involved in regulating interactions between actin and myosin in the muscle sarcomere and play a pivotal role in regulated muscle contraction. Nonmuscle tropomyosin isoforms function in both muscle and nonmuscle cells, and are involved in a range of cellular pathways that control and regulate the cell's cytoskeleton and other key cellular functions.

The actin filament system that is involved in regulating these cellular pathways is more complex than the actin filament systems that regulates muscle contraction. The contractile system relies upon 4 actin filament isoforms and 5 tropomyosin isoforms, whereas the actin filament system of the cytoskeleton uses two actin filament isoforms and over 40 tropomyosin isoforms.

Isoforms and evolution
In direct contrast with the 'one gene, one polypeptide' rule, it is now known from a combination of genomic sequencing, such as the Human Genome Project and EST data of expressed proteins, that many eukaryotes produce a range of proteins from a single gene. This plays a crucial role in the functionality of higher eukaryotes, with humans expressing more than 5 times as many different proteins (isoforms) as genes through alternative splicing. From a mechanistic point of view, it is much easier for an organism to expand on a current gene/protein family (creating protein isoforms) than it is to create an entirely new gene. From an evolutionary point of view, tropomyosins in higher eukaryotes are notable in retaining all 4 of the potential genes produced by the dual genomic duplication event that took place in early eukaryotic evolution.

Genes and isoforms (isoform complexity)
Within mammals, four genes are responsible for generating more than 40 different tropomyosin isoforms. In terms of structure, the genes are very similar, suggesting that they arose through gene duplication of an ancestral gene. In humans, these genes are no longer linked and are widely dispersed. In humans, the α1-, β-, α3-, and α4-genes are formally known as TPM1, TPM2, TPM3, and TPM4 and are located at 15q22, 9p13, 1q22 and 19p13, respectively. An alternative nomenclature names the four genes (α,β,γ,δ).

Isoforms are defined as highly related gene products that perform, in essence, similar biological functions, with variations existing between the isoforms in terms of biological activity, regulatory properties, temporal and spatial expression, and/or the intercellular location. Isoforms are produced by two distinct mechanisms, gene duplication and alternative splicing. The former mechanism is a process by which multiple copies of a gene are generated through unequal crossing over, through tandem duplication, or by translocation. Alternative splicing is a mechanism wherein exons are either retained in the mRNA or targeted for removal in different combinations to create a diverse array of mRNAs from a single pre-mRNA.

Splicing
A vast array of tropomyosin isoforms are generated by using a combination of different genes and alternative splicing. In mammals, regardless of the gene, transcription is initiated at the start of either exon 1a or exon 1b. Depending on the promoter and initial exon used, tropomyosin isoforms can be categorized as either high-molecular-weight (HMW, 284 amino acids) or low-molecular-weight (LMW, 248). HMW isoforms express exon 1a and either 2a or 2b, while LMW isoforms express exon 1b. To date, all known tropomyosins contain exons 3-9. Alternative splicing can occur at exon 6, with the mutually exclusive choice of exon 6a or 6b. At the c-terminus, the transcript is spliced again at exon 9, with the choice of exon 9a, 9b, 9c, or 9d.

Evolution of isoform generation
In terms of structure, the genes are very similar, suggesting that they arose through gene duplication of an ancestral gene. The most highly related genes are the α- and γ-genes, utilizing two promoters and differing only with the presence of the unique 2a exon in the α-gene. Although substantial differences between alternative exons from the same gene have been revealed by sequence comparison (1a and 1b, 6a and 6b, and the exon 9s), most exons are, however, highly conserved between the different genes. For example, exon 1a and 1b from the α-gene vary considerably in sequence; however, the sequence from exon 1a from the α-, β-, γ-, and δ-genes is highly conserved.

Due to the conservative nature of the genes, it is believed that the genes evolved from a common ancestral gene, giving rise to over 40 functionally distinct isoforms. The expression of these isoforms is highly regulated and variable throughout development. The diversity of tropomyosin expression, both in space and in time, provides the potential not only to regulate actin filament function but to create specialised actin filament populations.

Spatial sorting of tropomyosin isoforms
Numerous reports detail that tropomyosin isoforms are sorted to different intracellular locations, often associating with actin filament populations that are involved in specific processes. Direct visualization of spatial segregation of isoforms was initially observed by Burgoyne and Norman and soon after by Lin and co-workers. They observed that specific isoforms were associated with distinct cellular structures. Using specific antibodies, they were able to identify the presence of both HMW and the LMW isoforms of the γ-gene in stress fibers; however, only LMW isoforms were detected in ruffling membranes. These studies have been extended to a number of cell types with similar results. Extensive studies in neuronal cells, fibroblasts, skeletal muscle  and osteoclast cells has further highlighted the complex association tropomyosin isoforms have with cellular structures. These studies have led to the realization that the regulation of isoform sorting is extremely complex and highly regulated.

Regulation of sorting
Sorting of tropomyosin isoforms in discrete intracellular locations is developmentally regulated. Initial studies reported that the sorting of isoforms changed through development, where Tropomyosin 4 was initially localized to the growth cone of growing neurons, but in mature neurons it was relocated to the somatodendritic compartment. These observations have been supported by studies on different tropomyosin isoforms, showing how tropomyosin populations were relocated during neuron maturation. This evidence is supportive of the notion that tropomyosin isoforms are subject to temporal regulation.

Additional studies have identified the role the cell cycle plays in isoform sorting. A study that screened a range HMW products from the α- and β-genes and compared localisation with LMW products from the γ-gene found that the HMW and LMW products are mutually exclusively segregated during the early G1 phase of the cell cycle.

Mechanism of sorting
While studies suggest that tropomyosin sorting may be influenced by the sorting of mRNAs, there is no absolute correlation between mRNA and protein location. In neurons, Tropomyosin 5NM1 mRNA was found to sort to the pole of the neuron elaborating an axon prior to morphological differentiation. The sorting of Tropomyosin 5NM1/2 mRNA to this location correlated with the expression of the Tropomyosin 5NM1/2 protein. In contrast, the mRNA encoding the Tropomyosin Br2 protein was excluded from the pole of the neuron.

The link between mRNA sorting and protein location has been tested in transgenic mice models. The models were created so that the coding regions of Tropomyosin 5NM1/2 and Tropomyosin 3 were expressed under the control of the β-actin promoter with the a β-actin 3'-untranslated region lacking targeting information. The study found that Tropomyosin 3, an isoform that is not normally expressed in neuronal cells, was broadly distributed throughout the neuron, while exogenous expression of the neuronal isoform Tropomyosin 5NM1/2 was found to sort to the growth cone of neurons as does the endogenous Tropomyosin 5NM1/2. As these two transgenes differ only in the tropomyosin coding region yet are localized in two distinct areas, the findings suggest that, in addition to mRNA sorting, the proteins themselves contain sorting information.

Studies suggest that tropomyosin isoform sorting may also be influenced by the actin isoform composition of microfilaments. In myoblasts, overexpression of γ-actin resulted in the down-regulation of β–actin and the removal of Tropomyosin 2 but not Tropomyosin 5 from stress fibers. It was later found that, when cells were exposed to cytochalasin D, a chemical that results in the disorganization of actin filaments, tropomyosin isoform sorting was disrupted. Upon the washing out of cytochalasin D, tropomyosin isoform sorting was re-established. This is suggestive of a strong relationship between the process of tropomyosin isoform sorting and the incorporation of tropomyosin isoforms into organized arrays of actin filaments. There is no evidence for active transport of tropomyosin isoforms to specific locations. Rather, it appears that sorting is the result of local assembly of preferred isoforms at specific intracellular site. The mechanisms that underlie tropomyosin isoform sorting appear to be inherently flexible and dynamic in nature.

Isoforms are not functionally redundant
Many studies have led to the understanding that tropomyosins perform essential functions and are required in a diverse range of species from yeast, worms, and flies to complex mammals.

The essential role of tropomyosins was discovered in the Bretscher laboratory, where researchers found that, by eliminating the TPM1 gene of budding yeasts, growth rates were reduced, the presence of actin cables disappeared, defects in vesicular transport were observed, and mating of the yeast was poor. When a second yeast gene, TPM2, was deleted, no observable changes in the phenotype were recorded; however, when deleted in combination with TPM1, it resulted in lethality. This suggests that TPM1 and -2 genes have overlapping function; however, TPM2 cannot fully compensate of the loss of TPM1, indicating that some functions of TPM1 are unique. Similar results have been observed in flies, worms, amphibians, and mammals, confirming previous results and suggestive of tropomyosin's being involved in a wide range of cellular functions. However, the three co-expressed TMP1, 2, and 4 genes cannot compensate for deletion of the TPM3 gene in embryonic stem cells and preimplantation mouse embryos.

Results from gene knockout experiments can be ambiguous and must be carefully examined. In studies in which the deletion of a gene leads to lethality, it can at first appear that the gene product had a truly unique role. However, lethality can also be the result of the inability of the compromised cell to express other isoforms to rescue the phenotype because the required isoform is not naturally expressed in the cell.

Influencing binding of actin binding proteins to actin filaments
The actin microfilament system is the fundamental cytoskeletal system involved in the development and maintenance of cell morphology. The ability of this system to readily respond to cellular cues and undergo structural re-organisation has led to the belief that this system regulates specific structural changes within different cellular regions.

Within humans, there are only six actin isoforms, and these isoforms are responsible for an array of unique and complex cellular structures and key cellular interactions. It is thought that the function and form of the actin cytoskeleton is controlled largely by actin-binding proteins (ABP) that are associated with the actin polymer. ABP are a group of proteins that bind to actin. Although tropomyosin is sometimes included as an ABP, it is not a true ABP. The tropomyosin dimer has very low affinity for an actin filament and forms no van der waals contacts with actin. It is only the formation of a tropomyosin polymer's winding around the actin filament that provides stability to the tropomyosin-actin filament interaction.

Many studies suggest that the binding of tropomyosin isoforms to an actin filament may influence the binding of other ABPs, which together alter the structure and convey specific properties and ultimately specific functions to an actin filament. This is demonstrated in neuroepithelial cells, where increased expression of Tropomyosin 5NM1 increases the recruitment of myosin IIB, a myosin motor protein to the growth cone area. However, the over-expression of Tropomyosin Br3 had the opposite effect, decreasing myosin activity in the same region.

In a pioneering study by Bernstein and Bamburg, it was observed that the actin-binding protein actin depolymerisation factor (ADF)/cofilin, a factor that promotes actin filament depolymerisation, competed with tropomyosin for binding to the actin filament. The expression of Tropomyosin 5NM1 in neuronal cells eliminated ADF/cofilin from the growth cone region, leading to more stable actin filaments. However, the increased expression of Tropomyosin Br3 was observed to recruit ADF/cofilin to actin filaments bound to the Tropomyosin Br3 isoform within the lamellipodium, which led to the disassembly of actin filaments. This phenomenon, whereby a specific tropomyosin isoform directs specific interactions between actin-binding proteins, and the actin filament has been observed in a variety of model systems with a range of different binding proteins (reviewed in Gunning et al., 2008 ). These interactions, under the influence of tropomyosin isoforms, allow actin filaments to be involved in a diverse range of cellular functions.

Function in skeletal muscle contraction
Skeletal muscle is composed of large, multi-nucleated cells (muscle fibers). Each muscle fiber is packed with longitudinal arrays of myofibrils. Myofibrils are composed of repeating protein structures or sarcomeres, the basic functional unit of skeletal muscle. The sarcomere is a highly structured protein array, consisting of interdigitating thick and thin filaments, where the thin filaments are tethered to a protein structure, the Z-line. The dynamic interaction between the thick and thin filaments results in muscle contraction.

Myosin belongs to a family of motor proteins, and the muscle isoforms of this family comprise the thick filament. The thin filament is made of the skeletal muscle isoforms of actin. Each myosin protein 'paddles' along the thin actin filament, repeatedly binding to myosin-binding sites along the actin filament, ratcheting and letting go. In effect, the thick filament moves or slides along the thin filament, resulting in muscle contraction. This process is known as the sliding filament model.

The binding of the myosin heads to the muscle actin is a highly regulated process. The thin filament is made of actin, tropomyosin, and troponin. The contraction of skeletal muscle is triggered by nerve impulses that in turn stimulate the release of Ca2+. The release of Ca2+ from the sarcoplasmic reticulum causes an increase in the concentration of Ca2+ in the cytosol. Calcium ions then bind to troponin, which is associated with tropomyosin. Binding causes changes in the shape of troponin and subsequently causes the tropomyosin isoform to shift its position on the actin filament. This shifting in position exposes the myosin-binding sites on the actin filament, allowing the myosin heads of the thick filament to bind to the thin filament.

Structural and biochemical studies suggest that the position of tropomyosin and troponin on the thin filament regulates the interactions between the myosin heads of the thick filament and the binding sites on the actin of the thin filament. X-ray diffraction and cryoelectron microscopy suggest that tropomyosin sterically blocks the access of myosin to the actin filament.

Although this model is well-established, it is unclear as to whether the movement of tropomyosin directly causes the myosin head to engage the actin filament. As such, an alternative model has emerged, whereby the movement of the tropomyosin in the filament functions as an allosteric switch that is modulated by activating myosin binding but does not function solely by regulating myosin binding.

Regulation of contraction in smooth muscle
Smooth muscle is a type of non-striated muscle, and, unlike striated muscle, contraction of smooth muscle is not under conscious control. Smooth muscle may contract spontaneously or rhythmically and be induced by a number of physiochemical agents (hormones, drugs, neurotransmitters). Smooth muscle is found within the walls of various organs and tubes in the body such as the esophagus, stomach, intestines, bronchi, urethra, bladder, and blood vessels.

Although smooth muscles do not form regular arrays of thick and thin filaments like the sarcomeres of striated muscles, contraction is still due to the same sliding filament mechanism controlled by myosin crossbridges interacting with actin filaments. The thin filament of smooth muscle is made of actin, tropomyosin, caldesmon, and calmodulin. Within this type of muscle, caldesmon and calmodulin control the tropomyosin-mediated transition between on and off activity states. Caldesmon binds to actin, tropomyosin, calmodulin, and myosin, of which its interactions with actin are most important. The binding of caldesmon is strongly influenced by tropomyosin. Caldesmon is an inhibitor of actinomyosin ATPase and motility, and both actin binding and caldesmon inhibition are greatly enhanced in the presence of tropomyosin.

Smooth muscle contraction is initiated by the release of Ca2+. Ca2+ binds to and activates calmodulin, which then binds to caldesmon. This binding causes the caldesmon protein to disengage from the actin filament, exposing the myosin-binding sites on the actin filament. Myosin motor heads are phosphorylated by myosin light-chain kinase, allowing the myosin head to interact with the actin filament and cause contraction.

Role in cytoskeleton function
The cytoskeleton is an elaborate network of filaments required for the proper functioning of a range of cellular processes including cell motility, cell division, intracellular trafficking, and the maintenance of cell shape. The cytoskeleton is composed of three distinct filament systems: microtubules, intermediate filaments, and microfilaments (also known as the actin cytoskeleton). It is the dynamic interactions between these filaments that provide cells with unique structures and functions.

A number of regulatory mechanisms, employing many actin-binding proteins, have evolved to control the dynamics of the actin filament system. It is believed that tropomyosins play a pivotal role in this regulatory system, influencing the associations the actin filament has with other ABPs. Together, these associations confer specific properties on the filament, allowing these structures to be involved in a wide range of cellular processes, but also to rapidly respond to cellular stimuli.

Cancer
Many studies have shown that there are specific changes to the repertoire of tropomyosins expressed in cells that are undergoing cellular transformation. These highly reproducible results suggest that, during the process of cellular transformation, a process whereby a normal cell becomes malignant, there is a decreased synthesis of HMW tropomyosin isoforms. In the initial studies, transformation of rat embryo fibroblast cell line REF-52 and of normal rat kidney cells led to decreased synthesis of HMW tropomyosins. In both of these systems, the down regulation was contributed to a decrease in the mRNA levels. These early results suggested that tropomyosins played a critical role in facilitating certain processes that occurred during cell transformation, such as actin filament re-organisation and changes in cell shape. These studies have been reproduced in other laboratories and in other cell lines, with similar results (reviewed in Gunning et al., 2008 ).

Furthermore, studies have highlighted a link between tropomyosin isoform expression and the acquisition of metastatic properties. A study compared isoform expression between a low- and highly-metastatic Lewis lung carcinoma cell line. The study found that as cells become more metastatic, there is a marked decrease in the expression of HMW tropomyosin 2 protein and mRNA levels.

These results have been confirmed in primary tumors and human models. Studies in colon and bladder cancer found increased expression of the LMW tropomyosin Tropomyosin 5NM1. The elevated expression of this isoform has also been seen in transformed rat fibroblasts, and it is thought that this isoform is required for the motility of highly metastatic melanoma. In addition, elevated expression of Tropomyosin 4 has been linked with lymph node metastasis in breast cancer.

All of these studies suggest that changes in the expression and complement of tropomyosin isoforms are integral to cancer and cancer progression. The consensus is that, in general, cancer cells become more reliant on LMW tropomyosins as HMW tropomyosins disappear with increasing malignancy. This discovery has led to the development of novel anti-tropomyosin compounds as potential anti-cancer agents.

Autoimmunity
Tropomyosins have been implicated in the autoimmune disease ulcerative colitis, a disease of the colon that is characterised by ulcers or open sores. The link between this disease and tropomyosin was first acknowledged in a study that found blood serum taken from 95% of patients with ulcerative colitis contained antibodies that reacted positively to tropomyosin. Additional studies have confirmed these results, but also identify Tropomyosin 5 and Tropomyosin 1 as the primary tropomyosins involved in the pathogenesis of ulcerative colitis. Tropomyosin 5 has been related to the development of pouchitis in the ileal pouch following surgery for ulcerative colitis. The elevated number of IgG-producing cells in the colonic mucosa of ulcerative colitis patients is largely committed to producing IgG against Tropomyosin 5-related epitopes. Tropomyosin 5 is, therefore, capable of inducing a significant T-cell response. A physicochemical analysis of common structural motifs present in 109 human autoantigens revealed that tropomyosins have the highest number of such motifs, and thus a very high propensity to act as autoantigens.

In addition to the role tropomyosins play in ulcerative colitis, tropomyosin antibodies have also been reported in acute rheumatic fever and the inflammatory disorder Behcet's syndrome. In both instances, it is unclear as to whether these antibodies play a direct role in the pathogenesis of these human conditions or reflect the high antigenicity of tropomyosins released from compromised cells.

Muscle diseases
Nemaline myopathy is a muscle disease that is characterised by the presence of electron-dense rod bodies in skeletal muscle fibers. These electron-dense rod bodies are composed mainly of α-actinin and actin. The disorder is often clinically categorized into several groups, including mild (typical), intermediate, severe, and adult-onset; however, these distinctions are somewhat ambiguous, as the categories frequently overlap. Causative mutations have been detected in skeletal α-actinin, tropomyosin, nebulin, and troponin. Within humans, mutations in both the γ-Tropomyosin and β-Tropomyosin genes have been identified. No mutations in the α-Tropomyosin gene have been identified in this condition for humans.

Allergies
Tropomyosin is the primary protein responsible for shellfish allergies, including those to crustaceans and molluscs.

Tropomyosin also causes some cases of cockroach allergy.

Antibodies
Given the vast array of processes that this protein has been reported to be involved with, there is great interest in tropomyosin isoforms within the scientific community.

One way in which specific isoforms of this protein can be studied in detail is through the use of antibodies. These specific antibodies can be used in protein-blotting experiments and applied to cells or tissue sections and observed under a microscope. This allows researchers not only to determine the level or concentration of an isoform or a group of isoforms, but to also identify the cellular location of a particular isoform and associations with other cellular structures or proteins.

At the present time, there are many commercially available antibodies; however, many of these antibodies are sold with minimal information regarding the antigen used to raise the antibody and therefore, the isoform specificity; as such, some research groups develop their own antibodies. Before these antibodies can be used, they must be extensively characterised, a process whereby the specificity of the antibody is examined to ensure that the antibody does not cross-react with other tropomyosins or other proteins.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Tropomyosin


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The 36th Chamber of Shaolin

The 36th Chamber of Shaolin (also known as The Master Killer, Shaolin Master Killer and Shao Lin San Shi Liu Fang) is a 1978 Hong Kong kung fu film directed by Lau Kar-leung and produced by Shaw Brothers, starring Gordon Liu. The film follows a highly fictionalized version of San Te, a legendary Shaolin martial arts disciple who trained under the general Chi Shan.

The 36th Chamber of Shaolin is widely considered to be one of the greatest kung fu films and a turning point in its director's and star's careers. It was followed by Return to the 36th Chamber (1980), which was more comedic in presentation and featured Gordon Liu as the new main character with another actor in the smaller role of San Te, and Disciples of the 36th Chamber (1985).

Plot
A young student named Liu Yude is drawn by his activist teacher into the local rebellion against the Manchu government. The government officials, headed by the brutal General Tien Ta, however, quickly discover and suppress the uprising, liquidating the school and killing the students' friends and family members. Yude decides to seek vengeance and liberation for the people, and heads for the Shaolin temple to learn kung fu.

Wounded by Manchu henchmen during an escape, Yude reaches the temple and seeks sanctuary. Initially the monks reject him, since he is an outsider, but the chief abbot has mercy on the young man and lets him stay. One year later, Yude - now known as San Te - begins his martial arts training in the temple's 35 chambers, in each of which the temple's novices are trained in one aspect of the kung fu fighting arts.

The chambers shown in San Te's training are as follows (names of the chambers, if given, are from the subtitles and in quotation marks):
 * "35th Chamber": This is considered the highest-level chamber, representing enlightenment and wisdom, where the monks are reciting the Buddhist sutras from memory. During the session, the head master will randomly ask random monks a verse in the sutras and they must answer correctly or else they be asked to stand aside. According to head master, this chamber's purpose is to make the monks master the sutras properly to enable them unlock the power of Chi, which enables them perform devastating Kung Fu technique. When the head master of the chamber tells San Te to leave due to his ignorance of the sutras, San Te protests, only for the head master to knock him down from a distance using Chi. San Te flees the chamber, and agrees to start at the lowest level. This is also the chamber San Te is never able to reach by the end of the movie.
 * "First Chamber": This chamber teaches lightness and balance. Monks in training must jump on a bundle of sticks floating in a pool of water to reach the dining hall. Falling in the water requires the monk to dry his clothes off before entering the dining hall (by which time the food is all gone). San-Te trains hard to master the skill by balancing himself on rolling barrels and eventually succeed in crossing the bundle of sticks with just one leg. He is then promoted to train in the second chamber.
 * Third Chamber: This chamber trains arm strength. Monks must carry water in buckets with blades attached to their arms to keep the arms held straight out. The chamber also serves as the monastery's laundry to incorporate daily chores into the training.
 * Fourth Chamber: This chamber trains wrist strength. Monks must strike a gong with a very long weighted bamboo pole to the rhythm of the head master's striking his wooden fish while using the bottom end of the pole. San Te struggles to lift the pole at first so he starts with closed distance of the pole and gradually decreasing the distance of the pole until he is able to strike the gong with the bottom end of the pole.
 * Fifth Chamber: This chamber trains eyesight. Monks must follow a light without turning their heads, or risk getting burned by large sticks of incense. The final test will be for the trainees to strike the pillars with mirrors that reflect light from the candle at fast speed.
 * Sixth Chamber: This chamber trains head strength. Monks must headbutt their way through a corridor of sandbags and then place incense sticks on an altar while suffering from the concussion effect of the headbutts. This is the last conditioning chamber and in order to pass, one must remain stable after headbutting their way through the sandbags. After passing this chamber, San Te is allowed to learn kung fu techniques. Eventually San Te succeeds and is praised for completing all the basic trainings in less than two years.
 * Seventh Chamber: This is the chamber for training empty-hand forms and techniques.
 * "Leg Chamber": This chamber trains kicking techniques.
 * "Sword Chamber": This chamber trains broadsword techniques.
 * Ninth Chamber: This chamber trains staff techniques.

San Te advances more rapidly than any previous student, reaching the rank of deputy overseer within the space of six years. Challenged by the monastery's Discipline Chief, who thinks him unfit for his role, San Te has several exhibition matches with him, only to be beaten each time. However, after inventing the three section staff, San Te finally prevails and gains the chief abbot's permission to become overseer of one of the chambers.

When San Te professes that he wants to create a new chamber where he can train ordinary people in the basics of kung fu so they can defend themselves against their oppressors, the temple officially banishes him in a surreptitious way to allow him to carry out his mission. He returns to the outside world, namely to his hometown, and assists the people, gathering several young men who loyally follow him and become his first students. Before the political revolution where his aspirations reach completion, he is forced into conflict with Tien Ta. A fierce duel ensues, where San Te is victorious. Finally, he returns to the Shaolin temple, where he establishes the 36th chamber, a special martial arts class for laypeople to learn kung fu.

Cast

 * Gordon Liu as Liu Yude/Monk San Te
 * Lo Lieh as General Tien Ta
 * Wong Yue as Rice Miller Six
 * Yu Yang as Hung Hsi-Kuan
 * Norman Chu as Lu Ah-Tsai (as Hsu Shao-Chiang)
 * Wu Hang-Sheng as Tung Chien-Ching
 * Lee Hoi-sang as Abbot of Justice Office
 * Lau Kar-wing as General Yin (as Chia-Yung Liu)

Critical reception
36th Chamber of Shaolin received critical acclaim and is widely considered to be one of the greatest kung fu films ever made and a highly influential entry in the genre.

According to the Harvard Film Archive, the film is an "exhilarating rendition of the legendary dissemination of the Shaolin martial arts" and an "absorbing account of [an] initiation into the vaunted Shaolin style, ... depicted here [as] an inner voyage of discovery".

In 2014, Time Out polled several film critics, directors, actors and stunt actors to list their top action films; The 36th Chamber of Shaolin was listed in 22nd place on this list.

In 2021, Complex ranked The 36th Chamber of Shaolin number 5 in a list of the "24 Best Kung Fu Movies of All Time".

Home media
The 36th Chamber of Shaolin was released on VHS as early as 1993, under the title Master Killer. It was released on DVD in February 2000 by Crash Cinema Media as Shaolin Master Killer. In 2007, the film was released on DVD by The Weinstein Company's Asian label, Dragon Dynasty, as The 36th Chamber of Shaolin. In March 2010, Dragon Dynasty and Celestial Pictures released the film on Blu-ray.

On 6 December 2022, Arrow Video released The 36th Chamber of Shaolin on Blu-ray as part of the Shawscope Volume Two boxed set.

In popular culture
The Wu-Tang Clan's debut album Enter the Wu-Tang (36 Chambers) got the latter part of its name from the film. In addition, Wu-Tang Clan member Masta Killa takes his name from one of the film's alternate titles. Wu-Tang member and producer RZA also samples the film on Ol' Dirty Bastard's Return to the 36 Chambers: The Dirty Version ("Intro") and Method Man's Tical ("Meth vs. Chef", "I Get My Thang in Action", "Tical").

A clip from the movie appears in a 2023 animated movie Teenage Mutant Ninja Turtles: Mutant Mayhem in which the title characters were trained in martial arts by their father figure Master Splinter by showing them various video clips containing martial arts, including from other classic Shaw Brothers films.

title: The 36th Chamber of Shaolin


text:
Mic Michaeli

Gunnar Mathias "Mic" Michaeli (born 11 November 1962) is a Swedish musician best known as the keyboardist for the rock band Europe. Like many of the other Europe members he grew up in Stockholm suburb Upplands Väsby. He joined the band for their Wings of Tomorrow tour in 1984, taking vocalist Joey Tempest's place behind the keyboards.

Career
Michaeli has co-written several Europe songs; his most famous song is the hit ballad "Carrie" from the album The Final Countdown. The song was co-written by Michaeli and Tempest and was Europe's biggest hit in the U.S., reaching number 3 on the Billboard Hot 100 chart.

After Europe went on hiatus in 1992, Michaeli recorded and toured with bands like Brazen Abbot, Last Autumn's Dream and former Black Sabbath / Deep Purple vocalist Glenn Hughes. He also co-wrote three songs on Joey Tempest's third solo album, Joey Tempest, which was released in 2002.

Gear
Michaeli has used various instruments during his career, including a Roland JX-8P, Yamaha SY99, Korg CX-3 and a Hammond C3. Today he is using a Roland Fantom X7, Nord Lead 3 and a Nord Electro.

Personal life
In 1989, Michaeli married Mia Hertler. They divorced in 2001 after 12 years of marriage.

Michaeli is currently living in Stockholm. He has three children, Marcus, Moa and Matilda. He does not have any social media pages apart from the official ones for Europe listed on their website.

Europe

 * The Final Countdown (1986)
 * Out of This World (1988)
 * Prisoners in Paradise (1991)
 * Start from the Dark (2004)
 * Secret Society (2006)
 * Last Look at Eden (2009)
 * Bag of Bones (2012)
 * War of Kings (2015)
 * Walk the Earth (2017)

Other artists

 * Tone Norum – One of a Kind (1986)
 * Glenn Hughes – From Now On... (1994)
 * Glenn Hughes – Burning Japan Live (1994)
 * Brazen Abbot – Live and Learn (1995)
 * Brazen Abbot – Eye of the Storm (1996)
 * Brains Beat Beauty – First Came Moses, Now This... (1997)
 * Brazen Abbot – Bad Religion (1997)
 * Thore Skogman – Än Är Det Drag (1998)
 * Nikolo Kotzev – Nikolo Kotzev's Nostradamus (2001)
 * Brazen Abbot – Guilty as Sin (2003)
 * Last Autumn's Dream – Last Autumn's Dream (2003)
 * Bosses Vänner – Läget? (2007)
 * John Norum – Play Yard Blues (2010)

title: Mic Michaeli


text:
Aurora Quezon

Aurora Antonia Aragon Quezon (born Aurora Antonia Aragón y Molina; February 19, 1888 – April 28, 1949) was the wife of Philippine President Manuel Luis Quezon and the First Lady of the Philippines from 1935 to 1944. Although she is recognized as the second First Lady of the Philippines, she was actually the first spouse of a Philippine president to be addressed as such, the honorific being unknown in the Philippines prior to Manuel Quezon's presidency. Much beloved by Filipinos, Quezon was known for involvement with humanitarian activities and served as the first chairperson of the Philippine National Red Cross.

Five years after her husband's death, she and her daughter María Aurora ("Baby") were assassinated while they were en route to Baler to open a hospital dedicated to President Quezon. The province of Aurora was named in her memory.

Early life
Aurora Aragón was born on February 19, 1888, to Pedro Aragón and Zenaida Molina in the town of Baler, then in the District of El Príncipe, a part of the province of Nueva Ecija (at that time, Baler was the capital of Nueva Ecija). Her mother was a Filipina mestiza born through a Spanish priest, Father Jose Urbina de Esparragosa, who arrived in Baler from Esparragosa de la Serena, Cáceres Province, Spain in 1847 serving as the town's parish priest. Her father is a native of Laguna. She is the youngest of the 4 sisters, her older sisters are Maria, called by her siblings Kaka Malaki, Emilia, referred to Kaka Munti, and Amparo, referred to as Kaka Nanis. During the Philippine Revolution, her father was imprisoned by the colonial authorities for being suspected as being a member of the Katipunan; he would die in captivity. Among her tutors during her youth was her mother's sister (aunt), María Dolores Molina, who was the mother of her first cousin and future husband Manuel Luis Quezon. After her father's imprisonment, she was taken in by her aunt María Dolores and uncle Lucio, and she lived for a time under the same roof as her future spouse. After Manuel's own parents had died, he would stay with the Aragón family whenever he was in Baler.

After Pedro Aragón's death, his survivors, including daughter Aurora, had been cast into extreme poverty, surviving on subsistence farming. This experience was said to have shaped young Aurora's lifelong attitude of according equal treatment to everybody, no matter their status in life. The Aragón family later moved to Lucena where Manuel was then serving as the provincial fiscal of Tayabas. Aurora, who had wanted to become a school teacher, enrolled at the Philippine Normal College in Manila at the expense of her future husband, but had to stop her studies after two years due to her poor health.

Marriage and family
In 1907, Manuel Luis Quezon was elected to the Philippine Assembly. By 1916, he was elected to the Philippine Senate and as that chamber's president. Aurora often visited Quezon in Manila. In December 1918, they were married in Hong Kong. They had four children: María Aurora "Baby" (September 23, 1919 – April 28, 1949); María Zenaida "Nini" (April 9, 1921 – July 12, 2021); Luisa Corazón Paz (February 17, 1924 – December 14, 1924); and Manuel Lucio Jr. "Nonong" (June 23, 1926 – September 18, 1998). Luisa would die in infancy.

The marriage lasted until Quezon's death in 1944. It withstood despite Quezon's reputation as a libertine; the author Stanley Karnow described Aurora Quezon as finding "solace in prayer and the Philippine law against divorce". Still, Aurora has also been described as "a devoted wife and a strict but understanding mother". Quezon himself publicly extolled his wife as "my friend, companion and partner".

Political wife and First Lady

Within the first seventeen years of the marriage, Manuel Quezon emerged as a dominant figure in Philippine politics. His career reached its apex in 1935, when he was elected President of the Commonwealth of the Philippines. During her husband's political life, Aurora stayed in the background, involving herself with women's organizations such as the National Federation of Women's Clubs, of which she was the honorary chairperson.

Time described Aurora as "dignified and portly". The Quezons were the first presidential couple to reside in Malacañan Palace, but she spent as little time as possible there, preferring to stay in a "nipa house" in Malacañang Park or in her farm, Kaleidan, in Arayat, Pampanga. She nevertheless was an active First Lady, engaging herself in the campaign to give Filipino women the right of suffrage, which was achieved in 1937. She was particularly involved in managing the family's Arayat farm to demonstrate how social justice could be applied to landlord-tenant relationships in an agrarian setting. She was involved in the Girl Scouts of the Philippines and the Associación de Damas Filipinas, a noted orphanage in Manila. She was also the honorary president of another orphanage, the White Cross, located in San Juan.

President Quezon was re-elected in November 1941, but his presidency was immediately beset with crisis when Japan invaded the Philippines in the following month. Aurora accompanied her husband to Corregidor in December 1941, where the President was sworn in by Chief Justice José Abad Santos for his second term on December 30, 1941. For the next two months, the Quezon family remained in Corregidor where, despite the difficult living conditions, Aurora was said to have maintained her poise and kept up with a daily mass. In February 1942, they began their long journey via Australia to escape the Japanese and establish the Government in exile of the Commonwealth of the Philippines, finally reaching the United States in June 1942.

While in exile, Aurora devoted her time to the care of her ailing husband, who died in Saranac, New York, from tuberculosis on August 1, 1944. She then moved to California to await their return to the Philippines. She and her daughters volunteered as nurses for the Red Cross.

Postwar activity
When Aurora Quezon returned to the Philippines, she was voted a pension of 1,000 pesos a month by the Philippine Congress. She returned the check, explaining: "I feel that on account of ... countless war widows and orphans ... I should waive collection of a pension . . . I cannot, in good conscience, receive ... Government assistance when so many of my less fortunate sisters and their children are not yet taken care of. . . I know [if I accepted] I would not be keeping faith with the memory of my beloved husband. . . ." This act, it was said, "demonstrated why thousands of Filipinos regard her as a combination queen-mother and patron saint". Quezon was offered a slot in the Liberal Party senatorial slate for the 1946 elections, which she declined. She, however, endorsed the presidential candidacy of Manuel Roxas, who defeated her husband's vice-president and successor, Sergio Osmeña, to win the presidency.

In 1947, with the active support of Quezon, the Philippine National Red Cross was established as an independent Red Cross organization. She became the first Chairperson of the Philippine National Red Cross, holding the position until her death. She also was named as honorary vice-president of the Philippine Tuberculosis Society.

She continued to be involved in civic work, such as the efforts to rebuild the Antipolo Church. She received honorary doctorates from the University of Santo Tomas, and from the University of Michigan at Ann Arbor. She was likewise bestowed the Ozanam Award from the Ateneo de Manila University, and the Pro Ecclessia et Pontifice Cross from Pope Pius XII.

Assassination
On the morning of April 28, 1949, Quezon left her home to travel to her husband's hometown of Baler to open the Quezon Memorial Hospital. She had been cautioned about this trip beforehand due to the frequent insurgency activities in Central Luzon of the Hukbalahap, the military arm of the Communist Party of the Philippines. She shrugged off the threat, remarking on the morning of the trip, "[Hukbalahap Supremo] Taruc knows my white hair and he will not hurt me." Nonetheless, a convoy of thirteen vehicles, including two military jeeps full of armed soldiers, accompanied Quezon. Together with Quezon in her Buick sedan were her daughter "Baby", then a law student at the University of Santo Tomas, her son-in-law Felipe "Philip" Buencamino (husband of "Nini"), Quezon City mayor Ponciano Bernardo and retired Armed Forces Chief of Staff Major General Rafael Jalandoni.

They traveled along the Baler–Bongabon Road connecting Baler with Nueva Ecija, which Quezon herself inaugurated in 1940. At Quezon's request, her vehicle led the caravan, and it soon sped away from the military jeep immediately behind it. As Quezon's vehicle traversed the mountain road, it was blocked by a group of armed men. The men ignored the protestations from General Jalandoni and Mayor Bernardo that Quezon was in the vehicle, and machine-gun fire erupted from the side of the road and from the mountain slopes. It was later estimated that between 100 and 200 armed men had participated in the attack. Mrs. Quezon, her daughter, and Bernardo were killed instantly, while her son-in-law was mortally wounded. The soldiers in the convoy soon arrived at the scene and exchanged fire with the assailants, who were able to seize the valuables of the victims before fleeing the scene. In all, twelve members of the Quezon party and ten of the assailants were killed. There was national and international condemnation of the massacre. United States President Harry Truman was shocked and simply declared, "It was awful." A nine-day national mourning period was declared, and President Elpidio Quirino openly wept during the funeral. Quezon was buried at Manila North Cemetery. The mourners included her two surviving children, Manuel Jr. and Nini, who herself was widowed by the massacre. While no Philippine president has ever been assassinated, Aurora Quezon is one of three presidential spouses to have been murdered. (The other two were Alicia Syquia-Quirino and Senator Benigno Aquino Jr., both of whom died before their spouses were elected president.)

It was widely believed that the Hukbalahap was responsible for the killings. In preparation of the attack, the insurgents had blockaded the road and rounded up passengers from passing vehicles, and one of those passengers claimed seeing a former employee of his who had joined the Huk as among the armed men. While General Jalandoni, who survived the attack, tagged the Huks as responsible, the chief of the Philippine Constabulary laid blame instead on bandits. President Quirino blamed the Huks and responded by calling for "a people's war on the dissidents".

Luis Taruc, supremo of the Hukbalahap, denied that his group was responsible for the crime, though he also claimed that the Huk were conducting an investigation of their own if one of the group had breached ranks and participated in the killing. Nonetheless, after Taruc's surrender in 1954, he was formally charged for the murder of Quezon and other members of her party; these charges would be dropped before they could be heard on trial. Throughout the 1950s, several other captured Huk members would be charged for participation in the assassination, with five of them being sentenced to death by a Cabanatuan trial court. Luis Taruc later wrote the killings were discussed as an agenda item at the December 1949 to January 1950 Politburo meeting, "the accidental killing in a Huk ambush of Mrs. Quezon, widow of the late President Quezon, and her daughter. The majority took a characteristic Communist attitude toward this deplorable event. The victims had been 'class enemies', and that settled everything."

On April 28, 2005, exactly fifty-six years after her death, the remains of Quezon were transferred from North Cemetery for interment in a black crypt beside her husband's sarcophagus at the Quezon Memorial Shrine in Quezon City. The re-interment rites were attended by President Gloria Macapagal Arroyo and the Quezons' sole surviving child, Zenaida "Nini" Quezon-Avanceña.

Legacy
In 1951, Elpidio Quirino created the Aurora sub-province, named in her honor, comprising Baler and surrounding areas in the adjacent Quezon Province. A road that connects Manila and Quezon City via San Juan (then part of Rizal Province) was renamed Aurora Boulevard in her honor in 1963. In 1979, Aurora became a separate province. Manuel and Aurora Quezon are the only spouses to have respective provinces in the Philippines named after them. The first major building erected on Aurora Boulevard (also called Aurora Avenue), that is, the Aurora Tower at the Araneta Center in Cubao, was named after her. Her foremost legacy in the field of education was Mount Carmel College of Baler (formerly called Mount Carmel High School), a Catholic mission school founded in 1948 by American Carmelite missionaries who came to this town upon her invitation. The Concerned Women of the Philippines named the Aurora Aragon Quezon Peace Awards after her in 1988. The award was called the Human Rights Award in 1981, and winners included the Free Legal Assistance Group, the Agrava Commission, Jose W. Diokno, Claudio O. Teehankee, the MABINI law firm, and Cecilia Muñoz-Palma, but it was changed to focus on peace in 1988. Aurora A. Quezon Elementary School in Quezon City is also named for her, as well as the municipality of Aurora in Zamboanga del Sur. According to folktales, Doña Aurora Quezon wished to have a flower entitled to her, thus the 'Doña Aurora' (Mussaenda philippica) flower.

 * Aurora Quezon Day (19 February) – Celebrated throughout the provinces of Quezon and Aurora, and Lucena where it is a non-working holiday.

In popular culture

 * Portrayed by Rachel Alejandro in the film Quezon's Game (2019).

title: Aurora Quezon


text:
Talk:1993 Storm of the Century

Comments
I do not understand why this article speaks of the "shock" of such a strong storm. Everywhere I have looked has repeatedly stated how remarkably WELL forecast this storm was... — Preceding unsigned comment added by Famartin (talk • contribs) 05:45, 24 April 2005 (UTC)

 * ...I agree, I remember when this storm was coming very well, I was living in Upstate New York at the time, I remember people preparing for the storm for most of that week prior to the storm. (i.e. closing schools ahead of time before the storm even came, just as an example)I think they may have just underestimated how bad the storm was actually going to be though as opposed to the lack of coverage that the storm was coming. — Preceding unsigned comment added by 24.92.220.10 (talk) 17:54, 21 October 2005 (UTC)

 * I don't know about anywhere else, but the severity of the storm in Florida was a surprise until right before it hit. I was at my then-fiance's house in Tampa on the evening of the 12th watching TV when the 11 o'clock news began with an urgent weather bulletin and radar images of a vicious squall line approaching from the gulf. I hurried home before it hit. The next morning, the route back to her place was almost impassable with all kinds of debris. It had been forecast to be just a rainy night, but it obviously turned out to be a whole lot worse than than... Zeng8r 03:37, 11 August 2007 (UTC)

 * The article speaks to this issue. I also recall the storm coming and being warned and nobody could believe it (in Tennessee) until it happened.  It would have been an extreme storm for the south where it snowed even if it were in the middle of winter, so certainly so late was a very shocking event indeed. 76.90.49.187 17:58, 11 November 2007 (UTC)

Naming convention
Why does it have to have such a complex, pseudo-scientific name for the title? Having lived through the storm (I was in Florida, dodging tornadoes), I can tell you that EVERYBODY called this the Superstorm. --Kitch 11:09, 12 June 2006 (UTC)

 * Because, titleing the article "Superstorm" or "Storm of the Century" might cause confusion for some people. Although for the South it's defineitly the winner, people in New England and the West have different opinions on what the storm of the century is. Someguy-021 19:18, 10 July 2006 (UTC)Someguy-021

 * As a New Englander I can tell you that whenever I hear "Storm of the Century", I think of this event. Just my $0.02. — Preceding unsigned comment added by 138.69.160.1 (talk) 14:47, 2 February 2007 (UTC)

 * Yeah. This is one of the problems with naming extratropical cyclones.  I agree that the name should change to either Superstorm (1993) or Storm of the Century (1993).  In fact, if I remember my wikipedia page naming conventions correctly, since more people refer to/know of this storm as "Storm of the Century", it should be the article's name.  The current name cannot stand.  Thegreatdr 16:25, 2 February 2007 (UTC)

 * Done. Since it was an obvious change, and conforms to wikipedia naming standards better, I did not think it needed a vote of any sort.  Thegreatdr 16:32, 2 February 2007 (UTC)

 * Added "White Hurricane", as that's a common name in NC. In fact, having lived in NC since 1972, I'm a bit curious about the "No-Name Hurricane" moniker, as I've never heard anyone call that. Still - it's probably just a matter of local naming.  No specific objection - just an observation.  5minutes 16:48, 15 May 2007 (UTC)

Article merge with Subtropical Derecho
I definitely agree with such. It was the same system after all! CrazyC83 03:03, 27 September 2006 (UTC)

 * Emphatic Agree. Too lazy to do it now. Maybe tomorrow. -Runningonbrains 04:22, 27 September 2006 (UTC)

Storm table
I've made research on the web and able to produce a table of various snow amounts including the top amounts, amount on big cities and amounts in cities were snow is unusual. I've put one since some articles have listed storm amounts like this year's Valentine's Day blizzard in the northeast--JForget 19:59, 3 March 2007 (UTC)

 * I keep seeing sources that say that the panhandle of Florida had 6 inches of snow, but I can't find any specific location amount. Does anyone know of anywhere we could find that (with a verifiable link)? Gopher backer 01:53, 15 March 2007 (UTC)

 * Last I checked, the all time record for snow in Florida is 4 inches, set way back when the state border with Georgia was first surveyed in 1744 and then again in later years. I can tell you from going through this storm that the Florida panhandle did not receive more than a trace from this cyclone.  Measurable snow did penetrate rather far down into Georgia though.  Thegreatdr 07:53, 15 March 2007 (UTC)

 * Louisiana received some slush I doubt Florida got much more than that. 68.106.197.250 19:01, 15 June 2007 (UTC)

 * Actually I was in Alachua, Florida when this happened and we did infact, recieve a light coat of snow on the ground; not slush, snow. —Preceding unsigned comment added by 72.155.86.99 (talk) 16:25, 4 December 2008 (UTC)

 * Can you find a reliable source that confirms this? –Juliancolton Tropical Cyclone  16:35, 4 December 2008 (UTC)

WikiProject class rating
This article was automatically assessed because at least one WikiProject had rated the article as start, and the rating on other projects was brought up to start class. BetacommandBot 15:39, 29 August 2007 (UTC)

Requested move

 * The following discussion is an archived discussion of a requested move. Please do not modify it. Subsequent comments should be made in a new section on the talk page. No further edits should be made to this section.

The result of the move request was moved by December21st2012Freak. Jafeluv (talk) 09:21, 24 August 2009 (UTC)

Storm of the Century (1993) → 1993 Storm of the Century — More likely search term. – Juliancolton  | Talk 04:39, 22 August 2009 (UTC)

 * Support — proposed name is in compliance with Naming conventions (events). — V = I * R  (talk to Ω) 22:01, 22 August 2009 (UTC)

 * The above discussion is preserved as an archive of a requested move. Please do not modify it. Subsequent comments should be made in a new section on this talk page. No further edits should be made to this section.

Removed reference to "Perfect Storm"
I removed the reference to "the Perfect Storm" in this article as the writer erroneously thought that the book/movie referenced this 1993 blizzard, when in fact the book is about the 1991 Halloween "Perfect" storm (see wikipedia for entry). Marky1b (talk) 20:32, 8 December 2009 (UTC)

Major overhaul
There has been a significant rearrangement of material within the article. So far, nothing has been added, and very little has been removed. That which has been removed was meant to help the format of the article as a while, and bring it more inline with current wikipedia standards. It would be nice if someone can review the text, as I found much repetition within the article previously. Referencing would be helpful as well, which is what I'm working on right now. Thegreatdr (talk) 20:28, 21 December 2010 (UTC)

Aftermath
Why is it that the only thing that the "aftermath" section talks about is delays in nascar races? I think that would be fairly minor compared to some other things that would have happened in the aftermath. In fact, are the delays in the nascar races even notable enough to be mentioned? — Preceding unsigned comment added by 174.95.12.243 (talk) 08:33, 29 May 2011 (UTC)

Dead link
During several automated bot runs the following external link was found to be unavailable. Please check if the link is in fact down and fix or remove it in that case!

 * http://kyclim.wku.edu/factSheets/blizzard.htm
 * In 1993 Storm of the Century on 2011-05-25 06:05:38, HTTP Error: BadStatusLine
 * In 1993 Storm of the Century on 2011-06-24 20:07:50, HTTP Error: BadStatusLine

--JeffGBot (talk) 20:08, 24 June 2011 (UTC)

New Page at NWS
The National Weather Service has created a new page for the Superstorm of 1993. The new link is http://www.erh.noaa.gov/ilm/archive/Superstorm93/. Page Author: Tim Armstrong; Page Created: Feb 23, 2013. I also cited the deathtoll to this new page. — Preceding unsigned comment added by 108.195.179.49 (talk) 14:37, 7 May 2013 (UTC)

Important missing event
This storm sunk a ship on its way out by Canada. This was featured in a documentary about this storm and a few others in the North Sea, Irish Sea area that sunk a ferry and wiped out a coastal town in the Netherlands in the 1950's. The article List of shipwrecks in 1993 lists the Gold Bond Conveyor as foundering in the "Storm of the Century 1993". In the documentary there was harrowing footage taken from a search plane of the ship foundering, driving under successive waves until it finally did not come up, while in radio contact all the while.Jszigeti (talk) 13:33, 25 August 2014 (UTC)

Storm of the Century
Storm of the Century is a really uncyclopedic, overly sensacionalist and non-meteorological term, so I think that the term should be dropped quickly. I think that the name should be changed for something similar to Nor'easters or Blizzards. ABC paulista (talk) 03:10, 24 December 2014 (UTC)

Need clarification of some meteorological terms
Phrase like "strong shortwave trough" and "moved eastward into the Gulf of Mexico along a stationary front" may not make sense to lay persons. If it's stationary, how can it be moving? Shortwave is a kind of radio???

Perhaps someone knowledgable on these terms could clarify?

OliverHeaviside (talk) 19:46, 5 May 2015 (UTC)

External links modified
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 * Added archive https://web.archive.org/web/20110723153944/http://www2.sptimes.com/weather/SW.3.3.html to http://www2.sptimes.com/weather/SW.3.3.html
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Snowfall totals
Intro gives snowfall totals for mountains in NC (50") and TN (56"), but reverses the numbers farther down. — Preceding unsigned comment added by 2600:1700:E21:4730:443A:A8F9:4321:A9C2 (talk) 05:43, 8 November 2021 (UTC)

Complex wording
There is really no reason to use purely meteorological terms when discussing this event. It makes it unnecessarily difficult for a layperson, or someone unfamiliar with meteorology, to understand 2607:FEA8:FF01:6494:2D15:1EC5:BCD0:EFB6 (talk) 13:12, 28 July 2023 (UTC)

title: Talk:1993 Storm of the Century


text:
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 * To sign your posts (on talk pages, for example) use the '~' symbol. To insert just your name, type ~~~ (3 tildes), or, to insert your name and timestamp, use ~~~~ (4 tildes).
 * Try the Tutorial, and feel free to experiment in the test area.
 * If you need help, post a question at the Help Desk
 * Follow the Simplified Ruleset
 * Eventually, you might want to read the Manual of Style and Policies and Guidelines.
 * Remember Neutral point of view
 * Explore, be bold in editing pages, and, most importantly, have fun!

Good luck!

Meelar (talk) 05:46, Apr 24, 2005 (UTC)

Image copyright problem with Image:Donovan1.jpg
Thanks for uploading Image:Donovan1.jpg. However, the image may soon be deleted unless we can determine the copyright holder and copyright status. The Wikimedia Foundation is very careful about the images included in Wikipedia because of copyright law (see Wikipedia's Copyright policy).

The copyright holder is usually the creator, the creator's employer, or the last person who was transferred ownership rights. Copyright information on images is signified using copyright templates. The three basic license types on Wikipedia are open content, public domain, and fair use. Find the appropriate template in Image copyright tags and place it on the image page like this:.

Please signify the copyright information on any other images you have uploaded or will upload. Remember that images without this important information can be deleted by an administrator. If you have any questions, feel free to contact me, or ask them at the Media copyright questions page. Thank you. -- Gyrofrog (talk) 03:39, 23 December 2005 (UTC)

Image Tagging Image:Cantbuy.jpg
Thanks for uploading Image:Cantbuy.jpg. I notice the 'image' page currently doesn't specify who created the content, so the copyright status is therefore unclear. If you have not created this media yourself then you need to argue that we have the right to use the media on Wikipedia (see copyright tagging below). If you have not created the media yourself then you should also specify where you found it, i.e., in most cases link to the website where you got it, and the terms of use for content from that page.

If the media also doesn't have a copyright tag then you must also add one. If you created/took the picture, audio, or video then you can use GFDL-self to release it under the GFDL. If you believe the media qualifies as fair use, please read fair use, and then use a tag such as or one of the other tags listed at Image copyright tags. See Image copyright tags for the full list of copyright tags that you can use.

If you have uploaded other media, please check that you have specified their source and copyright tagged them, too. You can find a list of 'image' pages you have edited by clicking on the "my contributions" link (it is located at the very top of any Wikipedia page when you are logged in), and then selecting "Image" from the dropdown box. Note that any unsourced and untagged images will be deleted one week after they have been uploaded, as described on criteria for speedy deletion. Thank you. Shyam ( T / C ) 17:44, 3 March 2006 (UTC)

Image Tagging Image:Tripout.jpg
Thanks for uploading Image:Tripout.jpg. I notice the 'image' page currently doesn't specify who created the content, so the copyright status is unclear. If you have not created this media yourself then you need to argue that we have the right to use the media on Wikipedia (see copyright tagging below). If you have not created the media yourself then you should also specify where you found it, i.e., in most cases link to the website where you got it, and the terms of use for content from that page.

If the media also doesn't have a copyright tag then you must also add one. If you created/took the picture, audio, or video then you can use GFDL-self to release it under the GFDL. If you believe the media qualifies as fair use, please read fair use, and then use a tag such as or one of the other tags listed at Image copyright tags. See Image copyright tags for the full list of copyright tags that you can use.

If you have uploaded other media, please check that you have specified their source and copyright tagged them, too. You can find a list of 'image' pages you have edited by clicking on the "my contributions" link (it is located at the very top of any Wikipedia page when you are logged in), and then selecting "Image" from the dropdown box. Note that any unsourced and untagged images will be deleted one week after they have been uploaded, as described on criteria for speedy deletion. Thank you. Dethomas 03:33, 14 March 2006 (UTC)

Image copyright problem with Image:NaturalLogarithm.gif
Thanks for uploading Image:NaturalLogarithm.gif. However, the image may soon be deleted unless we can determine the copyright holder and copyright status. The Wikimedia Foundation is very careful about the images included in Wikipedia because of copyright law (see Wikipedia's Copyright policy).

The copyright holder is usually the creator, the creator's employer, or the last person who was transferred ownership rights. Copyright information on images is signified using copyright templates. The three basic license types on Wikipedia are open content, public domain, and fair use. Find the appropriate template in Image copyright tags and place it on the image page like this:.

Please signify the copyright information on any other images you have uploaded or will upload. Remember that images without this important information can be deleted by an administrator. If you have any questions, feel free to contact me. Thank you. --Adam Clark(User_Talk) (email) 20:48, 18 March 2006 (UTC)

Image copyright problem with Image:Paul Newman.jpg
Thanks for uploading Image:Paul Newman.jpg. However, the image may soon be deleted unless we can determine the copyright holder and copyright status. The Wikimedia Foundation is very careful about the images included in Wikipedia because of copyright law (see Wikipedia's Copyright policy).

The copyright holder is usually the creator, the creator's employer, or the last person who was transferred ownership rights. Copyright information on images is signified using copyright templates. The three basic license types on Wikipedia are open content, public domain, and fair use. Find the appropriate template in Image copyright tags and place it on the image page like this:.

Please signify the copyright information on any other images you have uploaded or will upload. Remember that images without this important information can be deleted by an administrator. If you have any questions, feel free to contact me. Thank you. Sherool (talk) 15:59, 19 March 2006 (UTC)

title: User talk:The Naturals