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Old Saxon

Old Saxon (altsächsische Sprache), also known as Old Low German (altniederdeutsche Sprache), was a Germanic language and the earliest recorded form of Low German (spoken nowadays in Northern Germany, the northeastern Netherlands, southern Denmark, the Americas and parts of Eastern Europe). It is a West Germanic language, closely related to the Anglo-Frisian languages. It is documented from the 8th century until the 12th century, when it gradually evolved into Middle Low German. It was spoken throughout modern northwestern Germany, primarily in the coastal regions and in the eastern Netherlands by Saxons, a Germanic tribe that inhabited the region of Saxony. It partially shares Anglo-Frisian's (Old Frisian, Old English) Ingvaeonic nasal spirant law which sets it apart from Low Franconian and Irminonic languages, such as Dutch, Luxembourgish and German.

The grammar of Old Saxon was fully inflected with five grammatical cases (nominative, accusative, genitive, dative, and instrumental), three grammatical numbers (singular, plural, and dual), and three grammatical genders (masculine, feminine, and neuter). The dual forms occurred in the first and second persons only.

Relation with other West Germanic languages
In the early Middle Ages, a dialect continuum existed between Old Dutch and Old Saxon, a continuum which has since been interrupted by the simultaneous dissemination of standard languages within each nation and the dissolution of folk dialects. Although they share some features, a number of differences separate Old Saxon, Old English, and Old Dutch. One such difference is the Old Dutch utilization of -a as its plural a-stem noun ending, while Old Saxon and Old English employ -as or -os. However, it seems that Middle Dutch took the Old Saxon a-stem ending from some Middle Low German dialects, as modern Dutch includes the plural ending -s added to certain words. Another difference is the so-called "unified plural": Old Saxon, like Old Frisian and Old English, has one verb form for all three persons in the plural, whereas Old Dutch retained three distinct forms (reduced to two in Middle Dutch).

Old Saxon (or Old Low German) probably evolved primarily from Ingvaeonic dialects in the West Germanic branch of Proto-Germanic in the 5th century. However, Old Saxon, even considered as an Ingvaeonic language, is not a pure Ingvaeonic dialect like Old Frisian and Old English, the latter two sharing some other Ingvaeonic characteristics, which Old Saxon lacked.

Relation to Middle Low German
Old Saxon naturally evolved into Middle Low German over the course of the 11th and 12th centuries, with a great shift from Latin to Low German writing happening around 1150, so that the development of the language can be traced from that period.

The most striking difference between Middle Low German and Old Saxon is in a feature of speech known as vowel reduction, which took place in most other West Germanic languages and some Scandinavian dialects such as Danish, reducing all unstressed vowels to schwa. Thus, such Old Saxon words like gisprekan (spoken) or dagō (days' – gen. pl.) became gesprēken and dāge.

Early developments
Old Saxon did not participate in the High German consonant shift, and thus preserves stop consonants p, t, k that have been shifted in Old High German to various fricatives and affricates. The Germanic diphthongs ai, au consistently develop into long vowels ē, ō, whereas in Old High German they appear either as ei, ou or ē, ō depending on the following consonant.

Old Saxon, alone of the West Germanic languages except for Frisian, consistently preserves Germanic after a consonant, e.g. hēliand "savior" (heilant, hǣlend, but háiljands). Germanic umlaut, when it occurs with short a, is inconsistent, e.g. hebbean or habbian "to have" (habban). This feature was carried over into the descendant-language of Old Saxon, Middle Low German, where e.g. the adjective krank (sick, ill) had the comparative forms krenker and kranker. Apart from the e, however, the umlaut is not marked in writing.

Consonants
The table below lists the consonants of Old Saxon. Phonemes written in parentheses represent allophones and are not independent phonemes.

Notes:

 * The voiceless spirants, , and gain voiced allophones (, , and ) when between vowels. This change is only faithfully reflected in writing for  (represented with letters such as $⟨ƀ⟩$ and $⟨u⟩$). The other two allophones continued to be written as before.
 * Fricatives were devoiced again word-finally. Beginning in the later Old Saxon period, stops became devoiced word-finally as well.
 * Most consonants could be geminated. Notably, geminated gave, and geminated  probably gave ; Geminated  resulted in.
 * Germanic *h is retained as in these positions and thus merges with devoiced.

Vowels
Notes:

 * Long vowels were rare in unstressed syllables and mostly occurred due to suffixation or compounding.

Diphthongs
Notes:

 * The closing diphthongs and  sometimes occur in texts (especially in Genesis), probably under the influence of Franconian or High German dialects, where they replace Old Saxon developments  and  (which evolved from Proto-Germanic  and ).
 * The situation for the front opening diphthongs is somewhat unclear in some texts. Words written with io in the Heliand, the most extensive record of Old Saxon writing, are often found written variably with ia or even ie in most other texts, notably the later ones. The diphthong eventually merges into in almost every Middle Low German dialect.
 * There also existed 'long' diphthongs, and . These were, however, treated as two-syllable sequences of a long vowel followed by a short one, not proper diphthongs.

Morphology
Unlike modern English, Old Saxon was an inflected language rich in morphological diversity. It kept five out of the six distinct cases of Proto-Germanic: the nominative, accusative, genitive, dative and (Vestigially in the oldest texts) instrumental.

Old Saxon also had three grammatical numbers (singular, and dual, and plural) and three grammatical genders (masculine, feminine, and neuter). The dual forms occurred in the first and second persons only and referred to groups of exactly two.

Nouns
Old Saxon nouns were inflected in very different ways following their classes. Here are the endings for dag, "day" an a-stem masculine noun:

At the end of the Old Saxon period, distinctions between noun classes began to disappear, and endings from one were often transferred to the other declension, and vice versa. This happened to be a large process, and the most common noun classes started to cause the least represented to disappear. As a result, in Middle Low German, only the former weak n-stem and strong a-stem classes remained. These two noun inflection classes started being added to words not only following the historical belonging of this word, but also following the root of the word.

Verbs
The Old Saxon verb inflection system reflects an intermediate stage between Old English and Old Dutch, and further Old High German. Unlike Old High German and Old Dutch, but similarly to Old English, it did not preserve the three different verb endings in the plural, all featured as -ad (also -iad or -iod following the different verb inflection classes). Like Old Dutch, it had only two classes of weak verb, with only a few relic verbs of the third weak class (namely four verbs: libbian, seggian, huggian and hebbian).

This table sums up all seven Old Saxon strong verb classes and the three weak verb classes:

It should be noticed that the third weak verb class includes only four verbs (namely libbian, seggian, huggian and hebbian); it is a remnant of an older and larger class that was kept in Old High German.

Syntax
Old Saxon syntax is mostly different from that of modern English. Some were simply consequences of the greater level of nominal and verbal inflection – e.g., word order was generally freer. In addition:
 * The default word order was verb-second, very close to that of modern Dutch or modern German.
 * There was no do-support in questions and negatives.
 * Multiple negatives could stack up in a sentence and intensify each other (negative concord), which is not always the case in modern English, modern Dutch, or modern German.
 * Sentences with subordinate clauses of the type "when X, Y" (e.g. "When I got home, I ate dinner.") did not use a wh-type conjunction, but rather used a th-type correlative conjunction (e.g. thô X, thô Y in place of "when X, Y"). The wh-type conjunctions were used only as interrogative pronouns and indefinite pronouns.
 * Similarly, wh- forms were not used as relative pronouns (as in "the man who saw me" or "the car which I bought"). Instead, an indeclinable word the was used, often in conjunction with the definite article (which was declined for case, number and gender).

Orthography
Old Saxon comes down in a number of different manuscripts whose spelling systems sometimes differ markedly. In this section, only the letters used in normalized versions of the Heliand will be kept, and the sounds modern scholars have traditionally assigned to these letters. Where spelling deviations in other texts may point to significant pronunciation variants, this will be indicated.

In general, the spelling of Old Saxon corresponds quite well to that of the other ancient Germanic languages, such as Old High German or Gothic.

 * c and k were both used for . However, it seems that, as in other West-Germanic dialects, when was followed by i or e, it had the pronunciation  or . The letters c and x were preferred for the palatalisations, k and even sometimes ch being rather used before u, o or a for  (kuning for  'king', modern köning ; crûci for  ; forsachistu for ).
 * g represented or its allophone : brengian  'to bring', seggian  'to say', wege  'way' (dative).
 * g seems, at least in a few dialects, to have had the pronunciation or  at the beginning of a word, only when followed by i or e. Thus we find giār  'year' and even gēr  'year', the latter betraying a strong Old Frisian influence.
 * h represents and its allophone : holt  'wood', naht  'night' (mod. nacht).
 * i is used for both the vowels and  and the consonant : ik  'I' (mod. ick, ik), iār  'year'.
 * qu and kw always represent : quāmun 'they came'.
 * s represented, and between two vowels also.
 * th is used to indicate : thōhtun 'they thought'. ð is used for, occasionally also written dh.
 * u represented the vowels and, or the consonant  ~ , which was denoted sporadically across manuscripts by either ⟨ƀ⟩, ⟨b⟩, ⟨u⟩, ⟨v⟩, or ⟨f⟩'.
 * uu was normally used to represent, predating the letter w.
 * z only appeared in a few texts due to Old High German influence.

Literature
Only a few texts survive, predominantly baptismal vows the Saxons were required to perform at the behest of Charlemagne. The only literary texts preserved are Heliand and fragments of the Old Saxon Genesis. There is also:

 * Beda homily (Homilie Bedas)
 * Credo (Abrenunciatio diaboli et credo) → Old Saxon baptismal vow.
 * Essener Heberegister
 * Old Saxon Baptismal Vow (Sächsisches Taufgelöbnis)
 * Penitentiary (altsächsische Beichte, altwestfälische Beichte)
 * Trierer Blutsegen
 * Spurihalz (Wiener Pferdsegen)
 * Wurmsegen (Wiener Wurmsegen) (
 * Psalms commentary (Gernroder Psalmenkommentar)

Text sample
A poetic version of the Lord's Prayer in the form of the traditional Germanic alliterative verse is given in Old Saxon below as it appears in the Heliand.

General

 * Euler, Wolfram (2013). Das Westgermanische – von der Herausbildung im 3. bis zur Aufgliederung im 7. Jahrhundert – Analyse und Rekonstruktion (West Germanic – from its Emergence in the 3rd up until its Dissolution in the 7th Century CE – Analyses and Reconstruction). 244 p., in German with English summary, London/Berlin 2013, ISBN 978-3-9812110-7-8.
 * Ringe, Donald R. and Taylor, Ann (2014). The Development of Old English – A Linguistic History of English, vol. II, 632p. ISBN 978-0199207848. Oxford.
 * Ringe, Donald R. and Taylor, Ann (2014). The Development of Old English – A Linguistic History of English, vol. II, 632p. ISBN 978-0199207848. Oxford.

Lexicons

 * Gerhard Köbler: Altsächsisches Wörterbuch, (5. Auflage) 2014. ("An Old Saxon Dictionary")
 * Gerhard Köbler: Altsächsisches Wörterbuch, (5. Auflage) 2014. ("An Old Saxon Dictionary")

title: Old Saxon


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List of ambassadors of the United States to the United Kingdom

The United States ambassador to the United Kingdom (known formally as, The Ambassador of the United States of America to the Court of St James's) is the official representative of the president of the United States and the American government to the monarch (Court of St. James's) and government of the United Kingdom. The position is held by Jane D. Hartley, who presented her credentials to Queen Elizabeth II on July 19, 2022.

The position is regarded as one of the most prestigious posts in the United States Foreign Service due to the "special relationship" between the United States and the United Kingdom. The ambassadorship has been held by various notable politicians, including five who would later become president: John Adams, James Monroe, John Quincy Adams, Martin Van Buren and James Buchanan. However, the modern tendency of American presidents (of both parties) is to appoint keen political fundraisers from previous presidential campaigns, despite the importance and prestige of the office.

The ambassador and executive staff work at the American Embassy in Nine Elms, London. The official residence of the ambassador is Winfield House in Regent's Park.

Duties
The ambassador's main duty is to present U.S. policies to the government of the United Kingdom and its people, as well as report British policies and views to the federal government of the United States. The ambassador serves as a primary channel of communication between the two nations and plays an important role in treaty negotiations.

The ambassador is the head of the United States' consular service in the United Kingdom. As well as directing diplomatic activity in support of trade, the ambassador is ultimately responsible for visa services and for the provision of consular support to American citizens in the UK and oversees cultural relations between the two countries.

Ministers (1785–1811)
Independent

Democratic-Republican

Democrat

Whig

Republican

John Adams is referred to as the first "ambassador". He is also referred to as the first "minister plenipotentiary". Plenipotentiary means "having full power"; a minister that has power to act for their country in all matters.

Ministers (1815–1893)
Diplomatic relations with what had now become the United Kingdom of Great Britain and Ireland were restored after the War of 1812. The Congress of Vienna (1815) established a uniform system of diplomatic rank. Under that system, the highest rank of "ambassador" was a personal representative of a sovereign, and the next rank of "minister", represented a government. As a republic, the United States maintained diplomatic relations with Britain at the rank of Envoy Extraordinary and Minister Plenipotentiary. The rank was colloquially known as Minister, and the position continued to be referred to as "United States Minister to Great Britain".

Ambassadors (1893–present)
Although France became a republic in 1870, the country continued to exchange ambassadors with other Great Powers. In 1893, the United States followed the French precedent and upgraded its relations with other Great Powers to the ambassadorial level. The United States Legation in London became the United States Embassy, and the United States Minister to Great Britain became the United States Ambassador to Great Britain.

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


text: User talk:81.207.51.62

title: User talk:81.207.51.62


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Wijhe

Wijhe is a village in the Dutch province of Overijssel. It is located in the municipality of Olst-Wijhe and is situated about 12 km south of Zwolle on the banks of the river IJssel.

Wijhe was a separate municipality until 2001, when it merged with Olst.

History & Sights
The first written record of Wijhe dates from the year 960 as "Wie." The village has a church built in the late-Gothic style, parts of which date from the 13th and 14th century. The windmill in the centre is still in working order. It was built in 1703 and is the oldest eight square mill in the province. To the north of Wijhe lies the hamlet of Herxen with a riverside nature reserve.

Wijhe has three estates: Hengevoorde containing a manor house, Het Nijenhuis with a castle and De Gelder. The last one is the private property of Baron De Vos van Steenwijk, but it is free for public access. Most of the De Gelder castle was destroyed during World War II.

Transportation

 * Railway station: Wijhe

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Athetosis

Athetosis is a symptom characterized by slow, involuntary, convoluted, writhing movements of the fingers, hands, toes, and feet and in some cases, arms, legs, neck and tongue. Movements typical of athetosis are sometimes called athetoid movements. Lesions to the brain are most often the direct cause of the symptoms, particularly to the corpus striatum. This symptom does not occur alone and is often accompanied by the symptoms of cerebral palsy, as it is often a result of this physical disability. Treatments for athetosis are not very effective, and in most cases are simply aimed at managing the uncontrollable movement, rather than the cause itself.

Signs and symptoms
Athetosis can vary from mild to severe motor dysfunction; it is generally characterized by unbalanced, involuntary movements of muscle and a difficulty maintaining a symmetrical posture. The associated motor dysfunction can be restricted to a part of the body or present throughout the body, depending on the individual and the severity of the symptom. One of the pronounced signs can be observed in the extremities in particular, as the writhing, convoluted movement of the digits. Athetosis can appear as early as 18 months from birth with first signs including difficulty feeding, hypotonia, spasm, and involuntary writhing movements of the hands, feet, and face, which progressively worsen through adolescence and at times of emotional distress. Athetosis is caused by lesions in several brain areas such as the hippocampus and the motor thalamus, as well as the corpus striatum; therefore children during the developmental age could possibly suffer from severe communication deficits such as speech impairment, hearing loss, and failed or delayed acquirement of sitting balance, although most people with athetosis have normal or near-normal intelligence.

Causes
Athetosis is a symptom primarily caused by the marbling, or degeneration of the basal ganglia. This degeneration is most commonly caused by complications at birth or by Huntington's disease, in addition to rare cases in which the damage may also arise later in life due to stroke or trauma. The two complications of particular interest are intranatal asphyxia and neonatal jaundice.

Asphyxia
Asphyxia directly causes basal ganglia damage due to lack of oxygen and therefore, insufficient nutrient supply. The lesions caused by asphyxia are most prominent on the caudate nucleus and the putamen. However, a less-studied consequence of the resulting hypoxia is its effect on the concentrations of the neurotransmitter dopamine within the synapses of neurons in the basal ganglia. Hypoxia leads to an increase in the extracellular dopamine levels and therefore, an increase in the activity of the dopaminergic neurons. Furthermore, this increase in extracellular concentration is not caused by an increase in the neurotransmitter synthesis, but instead on inhibiting its reuptake back into the neurons and glial cells. Therefore, there is an increased dopaminergic effect as dopamine remains in the synapse at higher concentrations leading to additional post-synaptic response. As a result, the uncontrollable writhing motions witnessed with athetosis deal with the over-activity of synapses within the basal ganglia.

Neonatal jaundice
Neonatal jaundice is the other chief complication that leads to the basal ganglia damage associated with this condition. Jaundice is caused by hyperbilirubinemia, or abnormally high levels of bilirubin in the blood. Bilirubin is usually bound to albumin immediately and sent to the liver. However, in neonatal jaundice, the concentration of bilirubin overwhelms that of albumin and some of the bilirubin remains unconjugated and can enter the brain through the blood–brain barrier. Normally bilirubin would not be able to diffuse across the blood–brain barrier, but in infants, the barrier is immature and has higher permeability. Bilirubin is toxic as it prevents the phosphorylation of many proteins, including synapsin I which binds vesicles in the presynaptic terminal. Therefore, it directly inhibits the exocytosis of neurotransmitters and severely hinders the synapses it affects. In autopsies of children who suffered from neonatal jaundice, chronic changes of neuronal loss, gliosis and demyelination were observed in the basal ganglia and more specifically within the globus pallidus.

Thalamic stroke
Another study was done where the onset of athetoid movement followed a thalamic stroke. The thalamus is part of a pathway that is involved with the cortical feedback loop in which signals from the cortex are relayed through the striatum, pallidus and thalamus before making it back to the cortex. The striatum receives excitatory inputs from the cortex and inhibits the pallidum. By doing so it frees the thalamus from pallidal inhibition allowing the thalamus to send excitatory outputs to the cortex. Therefore, the lesions to the thalamus or any other part of this feedback loop can result in movement disorders as they can alter the reactivity of one towards the other. Also, in a case of people with thalamic stroke, a majority suffered severe sensory deficits and ataxia. It is proposed that this loss of proprioception and the ensuing loss of synergic stabilization may also lead to abnormal movements, such as those dealt with in athetosis.

Treatments
There are several different treatment approaches to dealing with athetosis. The most common methods are the use of drugs, surgical intervention, and retraining movements of the afflicted person. It is suggested that training a person to relearn movements can be helpful in select situations. Though, generally, this type of treatment will not work, in certain cases it can be found to be very helpful in treating the symptom of athetosis.

Drugs can also be used in the treatment of athetosis, however their collective effectiveness is not very convincing. There is not a single drug that is a standard among treatment. Many different medicines can be used, including: Most instances of drug use where the symptoms seem to be lessened tend to be in more mild cases of athetosis.
 * trihexyphenidyl
 * benzatropine
 * Curare, though not practical due to respiratory paralysis
 * Tetrabenazine
 * Haloperidol
 * Thiopropazate
 * Diazepam

Treatment by surgical intervention can obviously have the most immediate impact, again however, it is not a cure-all. In patients that have cerebral palsy as the cause of their athetosis, it has been demonstrated that a subthalamotomy tends to help relieve the extent of athetosis in approximately half of patients. Additionally, late 19th and early 20th century surgical accounts state that athetosis can be relieved by the removal of a part of the cerebral motor cortex or by cutting a part of the posterior spinal roots. Patients who undergo surgical treatment to relieve the athetosis often see significant improvement in the control of their limbs and digits. While surgery is often very beneficial in the short term and can produce near immediate results, in the long term it has been seen that its effects are not incredibly long lasting.

Choreoathetosis
Chorea is another condition which results from damage to the basal ganglia. Similar to athetosis, it results from mutations affecting the pallidum inhibition of the thalamus as well as increased dopaminergic activity at the level of the striatum. Considering the etiology of both disorders are fairly similar, it comes as no surprise that chorea and athetosis can and usually do occur together in a condition called choreoathetosis.

Cerebral palsy
Athetosis is a commonly occurring symptom in the disease cerebral palsy. Of all people with the disease, between 16% and 25% of them actually exhibit the symptom of athetosis. A component of this is the finding that most often the symptoms that involve athetosis occur as a part of choreoathetosis as opposed to athetosis alone.

It is also noteworthy that the presence of athetosis in cerebral palsy (as well as other conditions) causes a significant increase in a person's basal resting metabolic rate. It has been observed that those who have cerebral palsy with athetosis require approximately 500 more Calories per day than their non-cerebral palsy non-athetoid counterpart.

Pseudoathetosis
Pseudoathetosis is a movement disorder, very similar to athetosis, in which the symptoms are not differentiable from those of actual athetosis, however the underlying cause is different. While actual athetosis is caused by damage to the brain, specifically in the basal ganglia, pseudoathetosis is caused by the loss of proprioception. The loss in proprioception is caused by damage to the area between the primary somatosensory cortex and the muscle spindles and joint receptors. Additionally, when observing an MRI, it can be seen that in the brain of a pseudoathetoid patient, lesions on the brain are not seen in the basal ganglia, the area that is oftentimes the cause of athetosis.

Social implications
Athetosis is characterized as a symptom that is present in many forms of central nervous system disorders that affect the body movement coordination, such as cerebral palsy. Children may struggle to engage in social communication, since the poor coordination of the tongue and mouth muscles can reduce their speech ability and hinder their social interaction to a greater degree. The caregivers of the affected children are encouraged to closely monitor their nutrition and growth and to provide them with hearing aids in order to relieve their symptoms as well as support their academic plans. A growing number of patients is shown to benefit from communication devices such as shorthand typing programs and computer speech devices, as well as simple picture boards.

Patients living with the disorder into their adulthood often have trouble being involved in daily activities such as eating, walking, dressing, as well as performing everyday tasks. They are consistently faced with challenges that limit their ability to live on their own. They are more reluctant to be involved in social activities and romantic relationships and more likely to develop poor self-esteem and self-image related to their physical limitations as well as cognitive disabilities, though such habitual thinking is shown to decline when they feel they are accepted and supported by their peers. Patients are also inclined to associate themselves with people who tend not to be engaged in physical activities, according to the September 2008 issue of "Journal of Physical Activity and Health".

History
The first noted case of athetosis was discovered by W. A. Hammond and described in his book Diseases of the Nervous System in 1871. Hammond was also the person who created the term "athetosis", Greek for "without position". In his initial description of athetosis, the extent of the uncontrolled movement was limited to the fingers and toes. In association with this, he noted that the patients' calves and forearms were oftentimes flexed and that movements were generally slow. Over the period of time leading into the late 20th century, the definition of athetosis was expanded to include movements of the neck, tongue, face, and even the trunk. Along with the expansion of the symptoms came the recognition that it was a part of many medical conditions, including cerebral palsy and stroke.

Research directions
As athetosis is relatively difficult to treat, efforts are being made to help those with the condition live and perform tasks more effectively and more efficiently. One such example of work that has been recently undertaken is a project to help those affected with athetosis to use a computer with more ease. Software for the control of the computer uses joysticks that perform linear filtering to aid in control.

An additional possible treatment option for those afflicted with the symptom is neurostimulation. Studies have begun, and in cerebral palsy patients affected with dystonia-choreoathetosis, it has been demonstrated that neurostimulation has been an effective treatment in lessening symptoms in patients. There has not been a tremendous amount of experimentation, though, in this as a possible treatment option.

title: Athetosis


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Cardiac action potential

Unlike the action potential in skeletal muscle cells, the cardiac action potential is not initiated by nervous activity. Instead, it arises from a group of specialized cells known as pacemaker cells, that have automatic action potential generation capability. In healthy hearts, these cells form the cardiac pacemaker and are found in the sinoatrial node in the right atrium. They produce roughly 60–100 action potentials every minute. The action potential passes along the cell membrane causing the cell to contract, therefore the activity of the sinoatrial node results in a resting heart rate of roughly 60–100 beats per minute. All cardiac muscle cells are electrically linked to one another, by intercalated discs which allow the action potential to pass from one cell to the next. This means that all atrial cells can contract together, and then all ventricular cells. Rate dependence of the action potential is a fundamental property of cardiac cells and alterations can lead to severe cardiac diseases including cardiac arrhythmia and sometimes sudden death. Action potential activity within the heart can be recorded to produce an electrocardiogram (ECG). This is a series of upward and downward spikes (labelled P, Q, R, S and T) that represent the depolarization (voltage becoming more positive) and repolarization (voltage becoming more negative) of the action potential in the atria and ventricles.

Overview
Similar to skeletal muscle, the resting membrane potential (voltage when the cell is not electrically excited) of ventricular cells is around −90 millivolts (mV; 1 mV = 0.001 V), i.e. the inside of the membrane is more negative than the outside. The main ions found outside the cell at rest are sodium (Na+), and chloride (Cl−), whereas inside the cell it is mainly potassium (K+).

The action potential begins with the voltage becoming more positive; this is known as depolarization and is mainly due to the opening of sodium channels that allow Na+ to flow into the cell. After a delay (known as the absolute refractory period), the action potential terminates as potassium channels open, allowing K+ to leave the cell and causing the membrane potential to return to negative, this is known as repolarization. Another important ion is calcium (Ca2+), which can be found inside the cell in the sarcoplasmic reticulum (SR) where calcium is stored, and is also found outside of the cell. Release of Ca2+ from the SR, via a process called calcium-induced calcium release, is vital for the plateau phase of the action potential (see phase 2, below) and is a fundamental step in cardiac excitation-contraction coupling.

There are important physiological differences between the pacemaker cells of the sinoatrial node, that spontaneously generate the cardiac action potential and those non-pacemaker cells that simply conduct it, such as ventricular myocytes). The specific differences in the types of ion channels expressed and mechanisms by which they are activated results in differences in the configuration of the action potential waveform, as shown in figure 2.

Cardiac automaticity
Cardiac automaticity also known as autorhythmicity, is the property of the specialized conductive muscle cells of the heart to generate spontaneous cardiac action potentials. Automaticity can be normal or abnormal, caused by temporary ion channel characteristic changes such as certain medication usage, or in the case of abnormal automaticity the changes are in electrotonic environment, caused, for example, by myocardial infarction.

Phases
The standard model used to understand the cardiac action potential is that of the ventricular myocyte. Outlined below are the five phases of the ventricular myocyte action potential, with reference also to the SAN action potential.

Phase 4
In the ventricular myocyte, phase 4 occurs when the cell is at rest, in a period known as diastole. In the standard non-pacemaker cell the voltage during this phase is more or less constant, at roughly -90 mV. The resting membrane potential results from the flux of ions having flowed into the cell (e.g. sodium and calcium), the flux of ions having flowed out of the cell (e.g. potassium, chloride and bicarbonate), as well as the flux of ions generated by the different membrane pumps, being perfectly balanced.

The activity of these pumps serve two purposes. The first is to maintain the existence of the resting membrane potential by countering the depolarisation due to the leakage of ions not at the electrochemical equilibrium (e.g. sodium and calcium). These ions not being at the equilibrium is the reason for the existence of an electrical gradient, for they represent a net displacement of charges across the membrane, which are unable to immediately re-enter the cell to restore the electrical equilibrium. Therefore, their slow re-entrance in the cell needs to be counterbalanced or the cell would slowly lose its membrane potential.

The second purpose, intricately linked to the first, is to keep the intracellular concentration more or less constant, and in this case to re-establish the original chemical gradients, that is to force the sodium and calcium which previously flowed into the cell out of it, and the potassium which previously flowed out of the cell back into it (though as the potassium is mostly at the electrochemical equilibrium, its chemical gradient will naturally reequilibrate itself opposite to the electrical gradient, without the need for an active transport mechanism).

For example, the sodium (Na+) and potassium (K+) ions are maintained by the sodium-potassium pump which uses energy (in the form of adenosine triphosphate (ATP)) to move three Na+ out of the cell and two K+ into the cell. Another example is the sodium-calcium exchanger which removes one Ca2+ from the cell for three Na+ into the cell.

During this phase the membrane is most permeable to K+, which can travel into or out of cell through leak channels, including the inwardly rectifying potassium channel. Therefore, the resting membrane potential is mostly equal to K+ equilibrium potential and can be calculated using the Goldman-Hodgkin-Katz voltage equation.

However, pacemaker cells are never at rest. In these cells, phase 4 is also known as the pacemaker potential. During this phase, the membrane potential slowly becomes more positive, until it reaches a set value (around -40 mV; known as the threshold potential) or until it is depolarized by another action potential, coming from a neighboring cell.

The pacemaker potential is thought to be due to a group of channels, referred to as HCN channels (Hyperpolarization-activated cyclic nucleotide-gated). These channels open at very negative voltages (i.e. immediately after phase 3 of the previous action potential; see below) and allow the passage of both K+ and Na+ into the cell. Due to their unusual property of being activated by very negative membrane potentials, the movement of ions through the HCN channels is referred to as the funny current (see below).

Another hypothesis regarding the pacemaker potential is the 'calcium clock'. Calcium is released from the sarcoplasmic reticulum within the cell. This calcium then increases activation of the sodium-calcium exchanger resulting in the increase in membrane potential (as a +3 charge is being brought into the cell (by the 3Na+) but only a +2 charge is leaving the cell (by the Ca2+) therefore there is a net charge of +1 entering the cell). This calcium is then pumped back into the cell and back into the SR via calcium pumps (including the SERCA).

Phase 0
This phase consists of a rapid, positive change in voltage across the cell membrane (depolarization) lasting less than 2 ms in ventricular cells and 10–20 ms in SAN cells. This occurs due to a net flow of positive charge into the cell.

In non-pacemaker cells (i.e. ventricular cells), this is produced predominantly by the activation of Na+ channels, which increases the membrane conductance (flow) of Na+ (gNa). These channels are activated when an action potential arrives from a neighbouring cell, through gap junctions. When this happens, the voltage within the cell increases slightly. If this increased voltage reaches the threshold potential (approximately −70 mV) it causes the Na+ channels to open. This produces a larger influx of sodium into the cell, rapidly increasing the voltage further to around +50 mV, i.e. towards the Na+ equilibrium potential. However, if the initial stimulus is not strong enough, and the threshold potential is not reached, the rapid sodium channels will not be activated and an action potential will not be produced; this is known as the all-or-none law. The influx of calcium ions (Ca2+) through L-type calcium channels also constitutes a minor part of the depolarisation effect. The slope of phase 0 on the action potential waveform (see figure 2) represents the maximum rate of voltage change of the cardiac action potential and is known as dV/dtmax.

In pacemaker cells (e.g. sinoatrial node cells), however, the increase in membrane voltage is mainly due to activation of L-type calcium channels. These channels are also activated by an increase in voltage, however this time it is either due to the pacemaker potential (phase 4) or an oncoming action potential. The L-type calcium channels are activated more slowly than the sodium channels, therefore, the depolarization slope in the pacemaker action potential waveform is less steep than that in the non-pacemaker action potential waveform.

Phase 1
This phase begins with the rapid inactivation of the Na+ channels by the inner gate (inactivation gate), reducing the movement of sodium into the cell. At the same time potassium channels (called Ito1) open and close rapidly, allowing for a brief flow of potassium ions out of the cell, making the membrane potential slightly more negative. This is referred to as a 'notch' on the action potential waveform.

There is no obvious phase 1 present in pacemaker cells.

Phase 2
This phase is also known as the "plateau" phase due to the membrane potential remaining almost constant, as the membrane slowly begins to repolarize. This is due to the near balance of charge moving into and out of the cell. During this phase delayed rectifier potassium channels (Iks) allow potassium to leave the cell while L-type calcium channels (activated by the influx of sodium during phase 0) allow the movement of calcium ions into the cell. These calcium ions bind to and open more calcium channels (called ryanodine receptors) located on the sarcoplasmic reticulum within the cell, allowing the flow of calcium out of the SR. These calcium ions are responsible for the contraction of the heart.

Calcium also activates chloride channels called Ito2, which allow Cl− to enter the cell. Increased calcium concentration in the cell also increases activity of the sodium-calcium exchangers, while increased sodium concentration (from the depolarisation of phase 0) increases activity of the sodium-potassium pumps. The movement of all these ions results in the membrane potential remaining relatively constant, with K+ outflux, Cl− influx as well as Na+/K+ pumps contributing to repolarisation and Ca2+ influx as well as Na+/Ca2+ exchangers contributing to depolarisation. This phase is responsible for the large duration of the action potential and is important in preventing irregular heartbeat (cardiac arrhythmia).

There is no plateau phase present in pacemaker action potentials.

Phase 3
During phase 3 (the "rapid repolarization" phase) of the action potential, the L-type Ca2+ channels close, while the slow delayed rectifier (IKs) K+ channels remain open as more potassium leak channels open. This ensures a net outward positive current, corresponding to negative change in membrane potential, thus allowing more types of K+ channels to open. These are primarily the rapid delayed rectifier K+ channels (IKr) and the inwardly rectifying K+ current, IK1. This net outward, positive current (equal to loss of positive charge from the cell) causes the cell to repolarize. The delayed rectifier K+ channels close when the membrane potential is restored to about -85 to -90 mV, while IK1 remains conducting throughout phase 4, which helps to set the resting membrane potential

Ionic pumps as discussed above, like the sodium-calcium exchanger and the sodium-potassium pump restore ion concentrations back to balanced states pre-action potential. This means that the intracellular calcium is pumped out, which was responsible for cardiac myocyte contraction. Once this is lost, the contraction stops and the heart muscles relax.

In the sinoatrial node, this phase is also due to the closure of the L-type calcium channels, preventing inward flux of Ca2+ and the opening of the rapid delayed rectifier potassium channels (IKr).

Refractory period
Cardiac cells have two refractory periods, the first from the beginning of phase 0 until part way through phase 3; this is known as the absolute refractory period during which it is impossible for the cell to produce another action potential. This is immediately followed, until the end of phase 3, by a relative refractory period, during which a stronger-than-usual stimulus is required to produce another action potential.

These two refractory periods are caused by changes in the states of sodium and potassium channels. The rapid depolarization of the cell, during phase 0, causes the membrane potential to approach sodium's equilibrium potential (i.e. the membrane potential at which sodium is no longer drawn into or out of the cell). As the membrane potential becomes more positive, the sodium channels then close and lock, this is known as the "inactivated" state. During this state the channels cannot be opened regardless of the strength of the excitatory stimulus—this gives rise to the absolute refractory period. The relative refractory period is due to the leaking of potassium ions, which makes the membrane potential more negative (i.e. it is hyperpolarised), this resets the sodium channels; opening the inactivation gate, but still leaving the channel closed. Because some of the voltage-gated sodium ion channels have recovered and the voltage-gated potassium ion channels remain open, it is possible to initiate another action potential if the stimulus is stronger than a stimulus which can fire an action potential when the membrane is at rest.

Gap junctions
Gap junctions allow the action potential to be transferred from one cell to the next (they are said to electrically couple neighbouring cardiac cells). They are made from the connexin family of proteins, that form a pore through which ions (including Na+, Ca2+ and K+) can pass. As potassium is highest within the cell, it is mainly potassium that passes through. This increased potassium in the neighbour cell causes the membrane potential to increase slightly, activating the sodium channels and initiating an action potential in this cell. (A brief chemical gradient driven efflux of Na+ through the connexon at peak depolarization causes the conduction of cell to cell depolarization, not potassium.) These connections allow for the rapid conduction of the action potential throughout the heart and are responsible for allowing all of the cells in the atria to contract together as well as all of the cells in the ventricles. Uncoordinated contraction of heart muscles is the basis for arrhythmia and heart failure.

Channels
Ion channels are proteins that change shape in response to different stimuli to either allow or prevent the movement of specific ions across a membrane. They are said to be selectively permeable. Stimuli, which can either come from outside the cell or from within the cell, can include the binding of a specific molecule to a receptor on the channel (also known as ligand-gated ion channels) or a change in membrane potential around the channel, detected by a sensor (also known as voltage-gated ion channels) and can act to open or close the channel. The pore formed by an ion channel is aqueous (water-filled) and allows the ion to rapidly travel across the membrane. Ion channels can be selective for specific ions, so there are Na+, K+, Ca2+, and Cl− specific channels. They can also be specific for a certain charge of ions (i.e. positive or negative).

Each channel is coded by a set of DNA instructions that tell the cell how to make it. These instructions are known as a gene. Figure 3 shows the important ion channels involved in the cardiac action potential, the current (ions) that flows through the channels, their main protein subunits (building blocks of the channel), some of their controlling genes that code for their structure, and the phases that are active during the cardiac action potential. Some of the most important ion channels involved in the cardiac action potential are described briefly below.

HCN channels
Hyperpolarization-activated cyclic nucleotide-gated channels (HCN channels) are located mainly in pacemaker cells, these channels become active at very negative membrane potentials and allow for the passage of both Na+ and K+ into the cell (which is a movement known as a funny current, If). These poorly selective, cation (positively charged ions) channels conduct more current as the membrane potential becomes more negative (hyperpolarised). The activity of these channels in the SAN cells causes the membrane potential to depolarise slowly and so they are thought to be responsible for the pacemaker potential. Sympathetic nerves directly affect these channels, resulting in an increased heart rate (see below).

The fast sodium channel
These sodium channels are voltage-dependent, opening rapidly due to depolarization of the membrane, which usually occurs from neighboring cells, through gap junctions. They allow for a rapid flow of sodium into the cell, depolarizing the membrane completely and initiating an action potential. As the membrane potential increases, these channels then close and lock (become inactive). Due to the rapid influx sodium ions (steep phase 0 in action potential waveform) activation and inactivation of these channels happens almost at exactly the same time. During the inactivation state, Na+ cannot pass through (absolute refractory period). However they begin to recover from inactivation as the membrane potential becomes more negative (relative refractory period).

Potassium channels
The two main types of potassium channels in cardiac cells are inward rectifiers and voltage-gated potassium channels.

Inwardly rectifying potassium channels (Kir) favour the flow of K+ into the cell. This influx of potassium, however, is larger when the membrane potential is more negative than the equilibrium potential for K+ (~-90 mV). As the membrane potential becomes more positive (i.e. during cell stimulation from a neighbouring cell), the flow of potassium into the cell via the Kir decreases. Therefore, Kir is responsible for maintaining the resting membrane potential and initiating the depolarization phase. However, as the membrane potential continues to become more positive, the channel begins to allow the passage of K+ out of the cell. This outward flow of potassium ions at the more positive membrane potentials means that the Kir can also aid the final stages of repolarisation.

The voltage-gated potassium channels (Kv) are activated by depolarization. The currents produced by these channels include the transient out potassium current Ito1. This current has two components. Both components activate rapidly, but Ito,fast inactivates more rapidly than Ito, slow. These currents contribute to the early repolarization phase (phase 1) of the action potential.

Another form of voltage-gated potassium channels are the delayed rectifier potassium channels. These channels carry potassium currents which are responsible for the plateau phase of the action potential, and are named based on the speed at which they activate: slowly activating IKs, rapidly activating IKr and ultra-rapidly activating IKur.

Calcium channels
There are two voltage-gated calcium channels within cardiac muscle: L-type calcium channels ('L' for Long-lasting) and T-type calcium channels ('T' for Transient, i.e. short). L-type channels are more common and are most densely populated within the T-tubule membrane of ventricular cells, whereas the T-type channels are found mainly within atrial and pacemaker cells, but still to a lesser degree than L-type channels.

These channels respond to voltage changes across the membrane differently: L-type channels are activated by more positive membrane potentials, take longer to open and remain open longer than T-type channels. This means that the T-type channels contribute more to depolarization (phase 0) whereas L-type channels contribute to the plateau (phase 2).

Conduction system
In the heart's conduction system electrical activity that originates from the sinoatrial node (SAN) is propagated via the His-Purkinje network, the fastest conduction pathway within the heart. The electrical signal travels from the sinoatrial node, which stimulates the atria to contract, to the atrioventricular node (AVN), which slows down conduction of the action potential from the atria to the ventricles. This delay allows the ventricles to fully fill with blood before contraction. The signal then passes down through a bundle of fibres called the bundle of His, located between the ventricles, and then to the Purkinje fibers at the bottom (apex) of the heart, causing ventricular contraction.

In addition to the SAN, the AVN and Purkinje fibres also have pacemaker activity and can therefore spontaneously generate an action potential. However, these cells usually do not depolarize spontaneously, simply because action potential production in the SAN is faster. This means that before the AVN or Purkinje fibres reach the threshold potential for an action potential, they are depolarized by the oncoming impulse from the SAN This is called "overdrive suppression". Pacemaker activity of these cells is vital, as it means that if the SAN were to fail, then the heart could continue to beat, albeit at a lower rate (AVN= 40-60 beats per minute, Purkinje fibres = 20-40 beats per minute). These pacemakers will keep a patient alive until the emergency team arrives.

An example of premature ventricular contraction is the classic athletic heart syndrome. Sustained training of athletes causes a cardiac adaptation where the resting SAN rate is lower (sometimes around 40 beats per minute). This can lead to atrioventricular block, where the signal from the SAN is impaired in its path to the ventricles. This leads to uncoordinated contractions between the atria and ventricles, without the correct delay in between and in severe cases can result in sudden death.

Regulation by the autonomic nervous system
The speed of action potential production in pacemaker cells is affected, but not controlled by the autonomic nervous system.

The sympathetic nervous system (nerves dominant during the body's fight-or-flight response) increase heart rate (positive chronotropy), by decreasing the time to produce an action potential in the SAN. Nerves from the spinal cord release a molecule called noradrenaline, which binds to and activates receptors on the pacemaker cell membrane called β1 adrenoceptors. This activates a protein, called a Gs-protein (s for stimulatory). Activation of this G-protein leads to increased levels of cAMP in the cell (via the cAMP pathway). cAMP binds to the HCN channels (see above), increasing the funny current and therefore increasing the rate of depolarization, during the pacemaker potential. The increased cAMP also increases the opening time of L -type calcium channels, increasing the Ca2+ current through the channel, speeding up phase 0.

The parasympathetic nervous system (nerves dominant while the body is resting and digesting) decreases heart rate (negative chronotropy), by increasing the time taken to produce an action potential in the SAN. A nerve called the vagus nerve, that begins in the brain and travels to the sinoatrial node, releases a molecule called acetylcholine (ACh) which binds to a receptor located on the outside of the pacemaker cell, called an M2 muscarinic receptor. This activates a Gi-protein (I for inhibitory), which is made up of 3 subunits (α, β and γ) which, when activated, separate from the receptor. The β and γ subunits activate a special set of potassium channels, increasing potassium flow out of the cell and decreasing membrane potential, meaning that the pacemaker cells take longer to reach their threshold value. The Gi-protein also inhibits the cAMP pathway therefore reducing the sympathetic effects caused by the spinal nerves.

Clinical significance
Antiarrhythmic drugs are used to regulate heart rhythms that are too fast. Other drugs used to influence the cardiac action potential include sodium channel blockers, beta blockers, potassium channel blockers, and calcium channel blockers.

title: Cardiac action potential


text:
Sophia Perovskaya

Sophia Lvovna Perovskaya (Со́фья Льво́вна Перо́вская; 13 September 1853 – 15 April 1881) was a Russian revolutionary and a member of the revolutionary organization Narodnaya Volya. She helped orchestrate the assassination of Alexander II of Russia, for which she was executed by hanging.

Life as a revolutionary
Perovskaya was born in Saint Petersburg, into an aristocratic family who were the descendants by the marriage of Elizabeth of Russia. Her father, Lev Nikolaievich Perovsky, was the military governor of Saint Petersburg. Her grandfather, Nikolay Perovsky, was a governor of Taurida. She spent her early years in the Crimea, where her education was largely neglected, but where she began reading serious books on her own. After the family moved to Saint Petersburg, Perovskaya entered the Alarchinsky Courses, a girls’ preparatory program. Here she became friends with several girls who were interested in the radical movement. She left home at the age of sixteen over her father's objections to her new friends. In 1871–1872, together with these friends, she joined the Circle of Tchaikovsky. In 1872–1873 and 1874–1877, she worked in the provinces of Samara, Tver, and Simbirsk. During this period, she received diplomas as a teacher and a medical assistant.

A prominent fellow member of the Circle of Tchaikovsky, Peter Kropotkin, said the following of Perovskaya: "In her moral conceptions she was a "", but not in the least of the sermon-preaching type. Perovskaya was a "populist" to the very bottom of her heart and at the same time a revolutionist, a fighter of the truest steel. She said to me once: "We have begun a great thing. Two generations perhaps will succumb in the task, and yet it must be done.""

In 1873, Perovskaya maintained several conspiracy apartments in Saint Petersburg for secret anti-tsarist propaganda meetings that had not been sanctioned by the authorities. In January 1874, she was arrested and placed in the Peter and Paul fortress in connection with the Trial of the 193. She was acquitted in 1877–1878. Perovskaya also took part in an unsuccessful attempt to free Ippolit Myshkin, a revolutionary and a member of Narodnaya Volya. In the summer of 1878, Perovskaya became a member of Zemlya i Volya, was soon arrested again, and banished to the Olonets Governorate. She managed to escape on her way to exile and went underground.

As a member of Zemlya I Volya, Perovskaya went to Kharkov in order to organize the liberation of political prisoners from the central prison. In the fall of 1879, she became a member of the Executive Committee and later a member of the administrative committee of Zemlya i Volya. Perovskaya propagandized among students, soldiers, and workers, took part in organizing the Worker's Gazette, and maintained ties with political prisoners in Saint Petersburg. In November 1879 she took part in an attempt to blow up the imperial train on its way from Saint Petersburg to Moscow. The attempt failed. On her return to Saint Petersburg she joined Narodnaya Volya.

Assassination of Alexander II
Perovskaya participated in preparing assassination attempts on Alexander II of Russia near Moscow (November 1879), in Odessa (spring of 1880), and Saint Petersburg (the attempt that eventually killed him, 1 March 1881). She was the closest friend and later the wife of Andrei Zhelyabov, a member of the executive committee of Narodnaya Volya. Zhelyabov was to have directed the bombing attack, with the group of four bomb-throwers - Ignacy Hryniewiecki, Nikolai Kibalchich, Timofey Mikhailov, and Nikolai Rysakov. However, when Zhelyabov was arrested two days prior to the attack, Perovskaya took the role.

The night before the attack, Perovskaya helped assemble the bombs.

On Sunday morning, 13 March [1 March, Old Style], the bomb-throwers gathered at the group's flat on Telezhnaya Street. At 9–10 AM, Perovskaya and Kibalchich each brought two missiles. Perovskaya would later relate that, before heading to the Catherine Canal, she, Rysakov and Hryniewiecki sat in a confectionery store located opposite of the Gostiny Dvor, impatiently waiting for the right time to intercept Alexander II's cavalcade. From there they parted ways and converged on the canal.

In the afternoon, the Tsar was returning by Catherine Canal in his carriage after watching the weekly military roll call. Perovskaya, by taking out a handkerchief and blowing her nose as a predetermined signal, dispatched the assassins to the canal. When the carriage was close enough for an attack, Perovskaya gave a signal, and Rysakov threw the bomb under the Tsar's carriage. The autocrat survived this first action because his carriage was bulletproof but the second bomb, thrown by Ignacy Hryniewiecki, dispatched him.

Hanging
Rysakov was captured, and while in custody, in an attempt to save his life, cooperated with the investigators. His testimony implicated the other participants, and the tsarist police apprehended Sophia Perovskaya, along with others, on 22 March. Rysakov established the identity of all prisoners. Although he knew many of them only by their party pseudonyms, he was able to describe the role they each had played.

Just before her trial, she wrote in a letter to her mother: "My darling, I implore you to be calm, and not to grieve for me; for my fate does not afflict me in the least, and I shall meet it with complete tranquility, for I have long expected it, and known that sooner or later it must come. [...] I have lived as my convictions dictated, and it would have been impossible for me to have acted otherwise."

Perovskaya, along with the other conspirators were tried by the Special Tribunal of the Ruling Senate on 26–29 March and sentenced to death by hanging. She was the first woman in Russia sentenced to death for terrorism.

On the morning of 15 April [3 April, Old Style], the prisoners were transported to the parade grounds of the Semenovsky Regiment, where the execution was set to take place. They were all dressed in black prison uniforms, and on their chests hung a placard with the inscription: "Regicide". Perovskaya, along with Mikhailov and Kibalchich, was placed on a cart that was drawn through the city by a pair of horses. The correspondent of the London Times estimated that the execution was attended by a hundred thousand spectators. When priests ascended the gallows to give the last rites, the convicts almost simultaneously approached them and kissed the crucifix. Once the priests withdrew, Zhelyabov and Mikhailov approached Perovskaya and they kissed each other good-bye. Perovskaya had turned away from Rysakov. Four other Pervomartovtsy, including Zhelyabov, were hanged with her.

Legacy
Three decades after her death, Perovskaya would become the inspiration for the Japanese feminist Kanno Sugako, who was involved in a 1910 plan to assassinate the Emperor Meiji. Kanno was also executed by hanging.

In 2018 the New York Times published a belated obituary for Perovskaya.

In literature

 * Henry Parkes was inspired by her to write the poem, The Beauteous Terrorist. Reproduced in full in ''The Beauteous Terrorist and Other Poems by Sydney Electronic Text and Image Service.
 * Moss, Walter G., Alexander II and His Times: A Narrative History of Russia in the Age of Alexander II, Tolstoy, and Dostoevsky. London: Anthem Press, 2002. Several chapters on Perovskaya. (available online )
 * Croft, Lee B. Nikolai Ivanovich Kibalchich: Terrorist Rocket Pioneer. IIHS. 2006. ISBN 978-1-4116-2381-1. Content on Perovskaya, including her father, mother, and her unmarked burial.
 * Jan Guillou uses Perovskaya in his book ”Men inte om det gälle din dotter” (”But not if it concerns your daughter”) as an example of how changes in political situation can alter the perception of a person between being a terrorist and a freedom fighter.

title: Sophia Perovskaya


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Wikipedia:Articles for deletion/Fifty tallest

Although I can appreciate the sentiment (trying to edit the table at Fifty tallest buildings in the USA can be a daunting task), we shouldn't have duplicate articles just because of the diffculty of editing. RickK 21:10, Jul 25, 2004 (UTC)
 * Agreed. Delete.  Postdlf 22:25, 25 Jul 2004 (UTC)
 * Delete. Spectatrix 01:39, 2004 Jul 26 (UTC)
 * Agreed. Delete.  SWAdair | Talk  02:51, 26 Jul 2004 (UTC)
 * "...Able to leap tall buildings in a single delete..." - UtherSRG 16:06, 26 Jul 2004 (UTC)
 * & if you want to edit but find the table code too daunting, put your remarks in the talk page & someone else will presumably insert if they are appropriate. -- Jmabel 00:43, Jul 29, 2004 (UTC)
 * Delete. -- Chuq 07:59, 29 Jul 2004 (UTC)
 * Delete -- The idea was in case people had a problem with the table format- bad idea. Greyengine5 07:49, 2004 Aug 15 (UTC)


text: User talk:66.82.9.52

title: User talk:66.82.9.52


text:
Fen Rivers Way

The Fen Rivers Way is a long distance footpath that spans a distance of 50 miles. It runs between the City of Cambridge and the town of King's Lynn in West Norfolk. It follows the course of the River Cam and River Great Ouse across the Fenland landscape into the Wash. It provides a small part of European Long Distance Path E2 which goes from Nice to Galway.

Description
The Fenland landscape is a man-made environment constructed over many centuries. This fertile land is dominated by agriculture and is dissected by dykes, draining ditches, rivers and embankments. The walk gives walkers the opportunity to see the Fenland's open landscape and skies that contribute to the character of the Fens. The walk has a number of points of historical and wildlife interest. The route passes close to five railway stations, offering opportunities for one-way walks of varying lengths.

The route
Starting from Cambridge, the route follows the River Cam with its banks and pastures fringed with weeping willow trees and out into the fens. The Cam Washes have been designated a Site of Special Scientific Interest because of their rare and special habitats and wildlife. Within this SSSI, otters can sometimes be seen. Approximately 17 miles north-east of Cambridge is Wicken Fen National Nature Reserve, where walkers will pass through the remains of a fragment of a Fenland wilderness of former times. Wicken Fen was the first nature reserve to be owned by the National Trust and has been in its care since 1899. Wicken Fen is a haven for birds, plants, insects and mammals. It can be explored by the traditional wide droves and lush green paths, including a boardwalk nature trail, giving access to several hides.

A little north of here, the River Cam joins the River Great Ouse. Next walkers approach the city of Ely. The magnificent Ely Cathedral and ancient city dominate the skyline for miles around. At the hamlet of Brandon Creek, the Great Ouse is joined by the River Little Ouse and the route enters the county of Norfolk.

The Great Ouse is now contained by flood banks and from these banks there are views of the surrounding countryside. Denver Sluice, being at the confluence of five watercourses, was first built across the river in 1651 as a focus of the flood defence system that protects the low lying Fens, although it had to be rebuilt after bursting in 1713. Nearby Denver Windmill is a fully restored 19th century windmill which lies on the path of the Roman Fen Causeway. The Ouse Washes are an internationally significant environment. Flooded in winter, they attract thousands of migrating wildfowl. From Denver the river is tidal, bringing with it subtle changes in scenery and habitat. Close by is the Relief Channel, the final link in the drainage system, completed in 1964. The two waterways meet at King's Lynn, the historic port on the edge of the Wash where the footpath ends.

Way markings
The route is marked with a small circular badge with a blue eel logo.

In 1995, Cambridge's local newspaper, The Cambridge Evening News, ran a competition for its children's Saturday Club, to name the route and design the logo. The winning entry naming the walk "Fen Rivers Way" with an eel as the logo, was submitted by Alexander Hunt from Teversham.

Further walks
There are four smaller circular walks along the Fen Rivers Way.
 * Wicken Fen Walk
 * Baits Bite Walk
 * Fenland Village Walk
 * The Cutters Walk

title: Fen Rivers Way


text:
Argyll (car)

Argyll was a Scottish motor car marque manufactured from 1899 to 1932, and again from 1976 to around 1990.

The original Argyll marque
Alex Govan founded The Hozier Engineering Company in 1899, and it was at this factory that the first Argyll Voiturette was produced; copied from the contemporary Renault, it featured a 2¾ hp de Dion engine and shaft-drive. 1901 models had an upgraded engine of 5 hp; cars made in 1902 were upgraded even further, using 8 hp units. Soon there appeared a 10 hp twin with radiator tubes forming the sides of the hood; in 1904 the company introduced a range of Aster-engined cars with front-mounted radiators. One of these was a 10 hp of 1985 cc; others were fours of 3054 cc, 3686 cc, and 4849 cc. All cars featured Govan's rather awkward gearbox, which had a T-shaped gate and separate reverse and change-speed levers. The company, by now named Argyll Motors Ltd. had now become Scotland's biggest marque and soon moved from its premises in Bridgeton, Glasgow to a grand, purpose-built factory in Alexandria, West Dunbartonshire. The Argyll Motor Works covered 12 acre, had its own railway line, and was opened in 1906 by John Douglas-Scott-Montagu, 2nd Baron Montagu of Beaulieu. However, the new factory was never used to capacity, and the company began to decline after Govan's death in 1907. It went into liquidation in 1908.

Production restarted in 1910, under a company now named Argylls Ltd., with a new range of cars including the famed "Flying Fifteen", and a six-cylinder model. The 12/14 was widely sold as a taxi even being exported to New York. Four-wheel brakes designed by J.M. Rubury of Argyll and patented on 18 March 1910 by Henri Perrot and John Meredith Rubury (Patent number 6807) were available from 1911 on, and in 1912 the single Sleeve valve engine designed by company director Baillie P. Burt and J. P. McCollum began production; the entire range featured Burt-McCollum engines by 1914.

In May 1914, Argylls submitted two water-cooled 6-cylinder inline aero-engines to the British War Office as part of a contest to select new aircraft engines. During the competition one of the engines broke its crankshaft. The other engine completed a six hour run test at full load winning a £100 prize. Ultimately the type was not selected for production.

Argylls changed hands in 1914 and the Alexandria factory was sold to the Royal Navy for torpedo production. Car production was resumed on a small scale in the original Bridgeton works under the control of John Brimlow who had previously run the repair department. The first product from the new company was a revival of the pre-war 15·9 hp model, now with electric starter but few were sold. In 1922, it was joined by a 1½-litre sleeve valve model and in 1926 by the 12/40 sports.

The company made a final appearance at the London Motor Show in 1927 and the last cars were probably made in 1928 though still advertised until Argyll closed in 1932.

The second Argyll era
The name was re-used in 1976 by a new company who made a mid-engined sports car, the Argyll GT, in Lochgilphead, Scotland.

The new manufacturing company was founded by Bob Henderson. The new car was named after the original Argyll of 1898, in honour of a grandfather of one of the investors who worked in the Argyll factory at Alexandria.

The only model was the mid-engined Argyll GT (or "Turbo GT"), which was based on a sturdy box section chassis with space frame clothed in a fibreglass bodyshell made next door to the old Arrol-Johnston factory in Dumfries by Solway Marine. The 1976 prototype car featured a turbocharged Rover V8 engine. A version with a turbocharged Saab engine was also mooted, but none were built. The suspension came from the Triumph 2500 and the gearbox was a ZF 5-speed unit. By undoing ten bolts, the entire rear end, suspension, gearbox and engine came away.

A production version of the car, which made its debut in 1983, had a non-turbocharged version of the Douvrin Euro V6 as used by Renault, Peugeot and others, together with a Renault 30 transaxle. A turbocharged V8 of 3.5 - 4.2 litres, together with the ZF transmission, was an option, but none were built. Other engine options were the Lancia Beta engine and transmission, and a Buick V6 which had started out as a stillborn Indycar engine. A top speed of 160 mph (ca. 260 km/h) with the turbo V8 was claimed but never ratified. The quoted price at launch was £25-30,000, which was comparable to the contemporary Ferrari 308 GTB. Production capacity was stated to be twelve cars a year, but none were sold. The silver version used for the launch and publicity material belonged to the company accountant and was virtually never driven.

title: Argyll (car)


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Banish (brand)

Banish is an American brand of skincare products founded by Daisy Jing in 2013. The line of products includes oils, microneedling kits, vitamin C serums, exfoliating masks and other treatments for acne scarring.

History
Prior to founding the company, Banish founder Daisy Jing created a YouTube channel called The Acne Channel, where she uploaded videos about her experiences with acne. Jing initially planned to study Pre-Med at Duke University in order to become a dermatologist, before switching her major. After discovering microneedling and vitamin C treatments, she began creating her own skin products in her kitchen. She founded Banish on September 25, 2013. Banish was on the Inc. 5000 list in 2017. In 2019, Jing discussed the experiences that led to founding Banish in a TEDx talk at Georgia Tech.

Products
Banish sells a starter kit that contains a vitamin C serum and facial mist, pumpkin enzyme and charcoal exfoliating masks, and a moisturizer. Banish also sells a microneedling tool known as the Banisher 2.0. The Banisher 2.0 uses gold-plated titanium bristles for microneedling. There is also a Banish "Fighter Gel" made from green tea extract and aloe.

title: Banish (brand)


text:
Representation theory of Hopf algebras

In abstract algebra, a representation of a Hopf algebra is a representation of its underlying associative algebra. That is, a representation of a Hopf algebra H over a field K is a K-vector space V with an action H × V → V usually denoted by juxtaposition ( that is, the image of (h,v) is written hv ). The vector space V is called an H-module.

Properties
The module structure of a representation of a Hopf algebra H is simply its structure as a module for the underlying associative algebra. The main use of considering the additional structure of a Hopf algebra is when considering all H-modules as a category. The additional structure is also used to define invariant elements of an H-module V. An element v in V is invariant under H if for all h in H, hv = ε(h)v, where ε is the counit of H. The subset of all invariant elements of V forms a submodule of V.

Categories of representations as a motivation for Hopf algebras
For an associative algebra H, the tensor product V1 ⊗ V2 of two H-modules V1 and V2 is a vector space, but not necessarily an H-module. For the tensor product to be a functorial product operation on H-modules, there must be a linear binary operation Δ : H → H ⊗ H such that for any v in V1 ⊗ V2 and any h in H,

 * $$hv=\Delta h(v_{(1)}\otimes v_{(2)})=h_{(1)}v_{(1)}\otimes h_{(2)}v_{(2)},$$

and for any v in V1 ⊗ V2 and a and b in H,

 * $$\Delta(ab)(v_{(1)}\otimes v_{(2)})=(ab)v=a[b[v]]=\Delta a[\Delta b(v_{(1)}\otimes v_{(2)})]=(\Delta a )(\Delta b)(v_{(1)}\otimes v_{(2)}).$$

using sumless Sweedler's notation, which is somewhat like an index free form of Einstein's summation convention. This is satisfied if there is a Δ such that Δ(ab) = Δ(a)Δ(b) for all a, b in H.

For the category of H-modules to be a strict monoidal category with respect to ⊗, $$V_1\otimes(V_2\otimes V_3)$$ and $$(V_1\otimes V_2)\otimes V_3$$ must be equivalent and there must be unit object εH, called the trivial module, such that εH ⊗ V, V and V ⊗ εH are equivalent.

This means that for any v in

 * $$V_1\otimes(V_2\otimes V_3)=(V_1\otimes V_2)\otimes V_3$$

and for h in H,

 * $$((\operatorname{id}\otimes \Delta)\Delta h)(v_{(1)}\otimes v_{(2)}\otimes v_{(3)})=h_{(1)}v_{(1)}\otimes h_{(2)(1)}v_{(2)}\otimes h_{(2)(2)}v_{(3)}=hv=((\Delta\otimes \operatorname{id}) \Delta h) (v_{(1)}\otimes v_{(2)}\otimes v_{(3)}).$$

This will hold for any three H-modules if Δ satisfies

 * $$(\operatorname{id}\otimes \Delta)\Delta A=(\Delta \otimes \operatorname{id})\Delta A.$$

The trivial module must be one-dimensional, and so an algebra homomorphism ε : H → F may be defined such that hv = ε(h)v for all v in εH. The trivial module may be identified with F, with 1 being the element such that 1 ⊗ v = v = v ⊗ 1 for all v. It follows that for any v in any H-module V, any c in εH and any h in H,

 * $$(\varepsilon(h_{(1)})h_{(2)})cv=h_{(1)}c\otimes h_{(2)}v=h(c\otimes v)=h(cv)=(h_{(1)}\varepsilon(h_{(2)}))cv.$$

The existence of an algebra homomorphism ε satisfying

 * $$\varepsilon(h_{(1)})h_{(2)} = h = h_{(1)}\varepsilon(h_{(2)})$$

is a sufficient condition for the existence of the trivial module.

It follows that in order for the category of H-modules to be a monoidal category with respect to the tensor product, it is sufficient for H to have maps Δ and ε satisfying these conditions. This is the motivation for the definition of a bialgebra, where Δ is called the comultiplication and ε is called the counit.

In order for each H-module V to have a dual representation V such that the underlying vector spaces are dual and the operation * is functorial over the monoidal category of H-modules, there must be a linear map S : H → H such that for any h in H, x in V and y in V*,

 * $$\langle y, S(h)x\rangle = \langle hy, x \rangle.$$

where $$\langle\cdot,\cdot\rangle$$ is the usual pairing of dual vector spaces. If the map $$\varphi:V\otimes V^*\rightarrow \varepsilon_H$$ induced by the pairing is to be an H-homomorphism, then for any h in H, x in V and y in V*,

 * $$\varphi\left(h(x\otimes y)\right)=\varphi\left(x\otimes S(h_{(1)})h_{(2)}y\right)=\varphi\left(S(h_{(2)})h_{(1)}x\otimes y\right)=h\varphi(x\otimes y)=\varepsilon(h)\varphi(x\otimes y),$$

which is satisfied if

 * $$S(h_{(1)})h_{(2)}=\varepsilon(h)=h_{(1)}S(h_{(2)})$$

for all h in H.

If there is such a map S, then it is called an antipode, and H is a Hopf algebra. The desire for a monoidal category of modules with functorial tensor products and dual representations is therefore one motivation for the concept of a Hopf algebra.

Representations on an algebra
A Hopf algebra also has representations which carry additional structure, namely they are algebras.

Let H be a Hopf algebra. If A is an algebra with the product operation μ : A ⊗ A → A, and ρ : H ⊗ A → A is a representation of H on A, then ρ is said to be a representation of H on an algebra if μ is H-equivariant. As special cases, Lie algebras, Lie superalgebras and groups can also have representations on an algebra.

title: Representation theory of Hopf algebras


text: User talk:68.48.59.91

title: User talk:68.48.59.91