History of Chechens in the Russian Empire

Chechnya was first incorporated as a whole into the Russian Empire in 1859 after the decades-long Caucasian War. Tsarist rule was marked by a transition into modern times, including the formation (or re-formation) of a Chechen bourgeoisie, the emergence of social movements, reorientation of the Chechen economy towards oil, heavy ethnic discrimination at the expense of Chechens and others in favor of Russians and Kuban Cossacks, and a religious transition among the Chechens towards the Qadiri sect of Sufism.
Deportation of Chechens to Turkey.
In the 1860, Russia commenced with forced emigration to ethnically cleanse the region. Tsar Alexander II forced the exile of millions of Caucasians (including at least 100,000 Chechens) in 1860–1866. Although Circassians were the main (and most notorious) victims (hence the "Circassian Genocide"), the expulsions also gravely affected other peoples in the region. It was estimated that 80% of the Ingush left Ingushetia for the Middle East in 1865. Lowland Chechens as well were evicted in large numbers, and while many came back, the former Chechen Lowlands lacked their historical Chechen populations for a long period until Chechens were settled in the region during their return from their 1944–1957 deportation to Siberia. The Arshtins, at that time a (debatably) separate people, were completely wiped out as a distinct group: according to official documents, 1,366 Arshtin families disappeared (i.e. either fled or were killed), and only 75 families remained. These 75 families, realizing the impossibility of existing as a nation of only hundreds of people, joined (or rejoined) the Chechen nation as the Erstkhoi tukkhum.
As Dunlop points out, the 100,000 Chechens who were exiled in 1860–1864 may have comprised over half the nation at that time, as in the 1896 Russian census, there were only 226,171 Chechens listed.
Attempts to return.
Some Chechens tried to return, but the Tsarist government refused to let them, even when they promised to convert to the Orthodox faith if they did. Nonetheless, some managed to return regardless.
Social trends.
Conversion to Qadiri Islam.
In the mid-1800s, the Qadiri sect of Sufism gained large numbers of followers among the Chechens (largely at the expense of the Nakshbandi sect). Eventually, an overwhelming majority of Chechens were Qadiri, separating them from their eastern neighbors in Dagestan who continued to follow the Nakshbandi sect. The "zikr", which later came to be seen as more of a "Chechen custom" than a "Muslim or Qadiri custom", is the circular dance accompanied with chanting or singing, and was largely specific to the Qadiri sect (although later it became more ethnic as non-Qadiris joined in). Finally, the Qadiri sect focused much more on individual salvation rather than the need to improve society (as the Nakshbandi did). For this reason, the Russian government initially viewed this mass transition with the hope that its allegedly less societal mindset would mean an end to Chechen resistance to their rule. However, in protest of unfavorable conditions, the Chechens rose up again in 1877–8, and the Qadiris played a major role in organizing the movement.
Land confiscation from the natives.
In 1864, trying to dissuade further resistance, Tsar Alexander II issued a decree regarding the Caucasians' "religion, adat [Caucasian local law customs], lands and woods" stating that they would be preserved and protected "in perpetuity for the peoples of the North Caucasus".
However, it did not take Alexander long to break this promise. The Russian government seized large swathes (hundreds of thousands of hectares) of the best farming land and the best wooded land, and gave them to Cossacks. Considerable land was also awarded to Russian soldiers who would later assimilate with the surrounding Cossacks, identifying themselves as Cossacks. These confiscations impoverished generations of Chechens and made large numbers of them land-hungry, sparking escalation of conflicts between Chechens and Cossacks. Chechens and Ingush clans in the area previously were forced to go without their traditional lands, and they maintained claims on the land throughout the whole period, jumping to reclaim the land as Russia receded in 1917.
Ethnic Discrimination.
Ethnic discrimination occurred in many forms against Chechens during the Tsarist era of Chechen history, largely due to the colonialist viewpoint of the Russian government, viewing Chechens as inferior, savage and subversive, one of many peoples who Russia had a "moral duty to civilize".
Judicial.
During the Tsarist period, Cossacks and Russians were tried for all crimes in civilian courts, usually being taken into custody by civil authorities. By contrast, Chechens and Ingush (as well as some other ethnic groups in the region) were dealt with exclusively by the military and tried in military courts, where they were typically given drastically harsher sentences, often death for crimes such as stealing food.
Land ownership.
In addition to the initial land seizures, long term Russian policies favored the acquisition of more and more land by Russians at the expense of Chechens. In 1912, in their own homeland (and not including the lands north of the Terek that are often considered part of Chechnya and are currently within its jurisdiction), Chechens and Ingush owned well less than half as much land as Terek Cossacks did, per capita. Chechens had 5.8 desyatinas on average, Ingush had 3.0, and Terek Cossacks had 13.6.
Socioeconomic and Demographic changes.
By the end of the 19th century, major oil deposits were discovered around Grozny (1893) which along with the arrival of the railroad (early 1890s), brought economic prosperity to the region (then administered as part of the Terek Oblast) for the oil-mining Russian colonists. The immigration of colonists from Russia brought about a three-way distinction between Chechens and Ingush on one hand, Cossacks on a second, and "other-towners" (inogorodtsy), namely Russians and Ukrainians, who came to work as laborers. A debatable fourth group, including Armenian bankers and richer Russians, and even some rich Chechens (such as Tchermoeff), arose later. Some Chechens got rich off oil, and the industry brought wealth to Chechnya, and (along with other factors) caused a growth of a Chechen bourgeoisie and intelligentsia.
Emergence of nationalism.
During the late 1860s and 1870s, a modest Chechen national awakening in literary circles occurred. The conflict with Russia and its final incorporation into the empire, however, brought about the formation of a modern, European, nationalist identity of some Chechen writers, though it ironically solidified their separation, mainly over politics, from the Ingush. The nation was held to be all-important, trumping religion, political belief, or any other such distinction. In 1870, Chakh Akhriev wrote a compilation of Chechen and Ingush fairy tales (called "Chechen fairytales"). In 1872, Umalat Laudaev, an early Chechen nationalist, recorded the contemporary customs of the Chechens. Following in his footsteps, Chakh Akhriev did the same for their "brothers", the Ingush, the following year.
Other notable early Chechen nationalists included Akhmetkhan, Ibraghim Sarakayev, and Ismail Mutushev. Later Tsarist-era Chechen nationalists include the five Sheripov brothers, among others. Among these, Sarakayev, Mutushev, Akhmetkhan and Danilbek Sheripov were notably democratic-minded writers, while Danilbek's younger brother, Aslanbek, would adopt communism.


Chemoaffinity hypothesis

The Chemoaffinity hypothesis states that neurons make connections with their targets based on interactions with specific molecular markers and, therefore, that the initial wiring diagram of an organism is (indirectly) determined by its genotype. The markers are generated during cellular differentiation and aid not only with synaptogenesis, but also act as guidance cues for their respective axon.
Sperry's experiments.
Roger Wolcott Sperry pioneered the inception of the Chemoaffinity Hypothesis following his 1960s experiments on the African Clawed Frog. He removed the eye of a frog and rotated it 180°, Sperry then replaced the eye and the visual nervous system repaired itself. However, the frog now had inverted vision. Initial eye orientation gives that the top of the eye is Dorsal, and the bottom is Ventral. Post-operation, the "top" of the eye is now Ventral, and the bottom is Dorsal. When a food source was above the frog, it extended its tongue downwards; meaning that the Dorsal-Ventral orientation of the eye still remained. In follow up experiments, the eye was detached and rotated 180° and the optic nerve was also cut to see if this would affect the Dorsal-Ventral orientation. The results were identical.
Sperry concluded that each individual optic nerve and tectal neuron used some form of chemical marker which dictated their connectivity during development. He reasoned that when the eye had been rotated, each optic fiber and each tectal neuron possessed cytochemical labels that uniquely denoted their neuronal type and position and that optic fibers could utilize these labels to selectively navigate to their matching target cell, hence the visuomotor impairment.


Undercover Brother

Undercover Brother is a 2002 American satirical spy action comedy blaxploitation film directed by Malcolm D. Lee and starring Eddie Griffin. The screenplay is by Michael McCullers and co-executive producer John Ridley, who created the original Internet animation characters. It spoofs blaxploitation films of the 1970s as well as a number of other films, most notably the James Bond franchise. It also stars former "Saturday Night Live" cast member Chris Kattan and comedian Dave Chappelle as well as Aunjanue Ellis, Neil Patrick Harris, Denise Richards, and Billy Dee Williams, and features a cameo by James Brown.
Plot.
The film begins with a backstory of how African-American culture's popularity with the American public began to decline in the 1980s, when style and originality began to lose appeal in the public eye due to the persistent efforts of "The Man" (Robert Trumbull), a powerful Caucasian man in control of a secret organization that seeks to undermine the African-American community as well as the cultures of other minorities. The Man is infuriated that Gen. Warren Boutwell (Billy Dee Williams), a United States Army general based on Colin Powell, is considering running for president, and his lackey Mr. Feather (Chris Kattan) informs him of a mind-control drug which The Man uses to make Boutwell abort his plans and instead open a fried chicken franchise. The B.R.O.T.H.E.R.H.O.O.D., a secret organization that battles The Man's influence, determines The Man is behind Boutwell's change of heart, and recruits a freelance agent named Undercover Brother (Eddie Griffin) to aid them.
Undercover Brother joins B.R.O.T.H.E.R.H.O.O.D. which is made up of the Chief (Chi McBride), Conspiracy Brother (Dave Chappelle), Smart Brother (Gary Anthony Williams), Sistah Girl (Aunjanue Ellis), and Lance (Neil Patrick Harris), an intern who is the only white man in the organization due to affirmative action. Undercover Brother goes undercover as a new employee at a cigarette company owned by The Man, where Mr. Feather discovers his identity. He deploys a secret weapon that he calls "Black Man's Kryptonite", an attractive assassin named White She-Devil (Denise Richards). Posing as another new employee, she and Undercover Brother start dating, and she begins to make him do stereotypical "white" things, such as buying corduroy and khaki clothes, singing karaoke, and adopting a silly set of euphemisms. Meanwhile, The Man distributes his mind-control drug through Boutwell's fried chicken, infecting other black celebrities and making them act white.
Concerned with Undercover Brother's unusual behavior, Sistah Girl attacks White She-Devil and convinces Undercover Brother to return to the fight. White She-Devil turns on her own henchmen to save the two, revealing she has fallen in love with Undercover Brother. They return to the B.R.O.T.H.E.R.H.O.O.D., where Smart Brother questions White She-Devil about The Man and Lance is officially made part of the group when he declares his desire to abolish bigotry after watching "Roots". The group heads to an awards gala after they find out that James Brown is The Man's next target. Mr. Feather kidnaps Brown and takes him to The Man's base. B.R.O.T.H.E.R.H.O.O.D. secures an antidote for the mind control drug and follows via a transmitter placed on Brown, infiltrating the base posing as a cleaning crew, to rescue Brown and a mysterious "Candidate" that The Man plans to use to land a crushing blow to African-American culture.
Mr. Feather prepares to administer the drug to Brown and present him as a trophy to The Man, and Brown reveals himself as Undercover Brother in disguise. Mr. Feather sends his henchmen after B.R.O.T.H.E.R.H.O.O.D., who discover the Candidate is Boutwell, and is ordered by Mr. Feather to kill Undercover Brother. In the fighting, Conspiracy Brother accidentally begins the building's self-destruct sequence. The B.R.O.T.H.E.R.H.O.O.D. cures Boutwell and evacuate him from the building while Undercover Brother chases Mr. Feather to the roof. The Man's helicopter circles overhead and leaves, The Man abandoning Mr. Feather for failing him. Mr. Feather jumps onto the helicopter's landing gear as it flies away, and Undercover Brother uses his afro picks to impale Mr. Feather in the buttocks, causing him to fall into the ocean, where he is eaten by a shark. However, The Man escapes. Undercover Brother survives the building's self-destruction by leaping off the building and using his wide pants legs as parachutes. He and Sistah Girl kiss and leave the island, the world at peace.
There are several mid-credits scenes.
Filming locations.
The R. C. Harris Water Treatment Plant in Toronto served as the headquarters for "The Man".
Reception.
On Rotten Tomatoes, the film holds an approval rating of 77% based on 130 reviews, with an average rating of 6.8/10. The website's critics consensus reads, "Fast-paced and filled with racial gags, "Undercover Brother" serves up plenty of laughs and sharp satire." On Metacritic the film received a weighted average score of 69 out of 100, based on 30 critics, indicating "generally favorable reviews".
Mick LaSalle of the "San Francisco Chronicle" gave a positive review, stating: "The picture is crammed with shameless satire, engaging moments of pure silliness and jokes that border on the outrageous. It combines relentless energy with an aura of good nature for a formula that works."
Sequel.
A sequel titled "Undercover Brother 2" starring Michael Jai White, Gary Owen, Affion Crockett, and Brandon Hirsch was released on Netflix in 2019. The film was criticized for the unfunny script and being an unnecessary/dud sequel.


Fixed income analysis

Fixed income analysis is the process of determining the value of a debt security based on an assessment of its risk profile, which can include interest rate risk, risk of the issuer failing to repay the debt, market supply and demand for the security, call provisions and macroeconomic considerations affecting its value in the future. It also addresses the likely price behavior in hedging portfolios. Based on such an analysis, a fixed income analyst tries to reach a conclusion as to whether to buy, sell, hold, hedge or avoid the particular security.
Fixed income products are generally bonds: debt instruments requiring the issuer (i.e. the debtor or borrower) to repay the lender the amount borrowed (principal) plus interest over a specified period of time (coupon payments) until maturity. They are issued by government treasuries, government agencies, companies or international organizations.
Calculating Value.
To determine the value of a fixed income security, the analyst must estimate the expected cash flows from the investment and the appropriate required yield. The cash flows consist of:
The required yield is determined by investigating the yield offered on securities of comparable risk in the market. The required yield is applied to the expected cash flows to estimate their present value, which equals the security's value.
Analysis.
Key factors considered in fixed income analysis include the following:
The approaches for analysing fixed income products include the fundamental approach, the technical approach, and the relative value approach.


Periarchicortex

Periarchicortex is one of two subtypes of periallocortex, the other being peripaleocortex. It is formed at borders between archicortex (a subtype of allocortex) and isocortex and shows slow histological transition from the four-layered structure typical for archicortex to the six-layered structure typical for isocortex.
Cortical areas that are generally considered to belong to periarchicortex, include presubiculum, parasubiculum, entorhinal cortex, perirhinal cortex, retrosplenial cortex, periarchicortical part of cingulate cortex, posterior part of subcallosal area, and subgenual area.
Periarchicortex does not contact immediately at borders with the true isocortex and does not transit directly into it. Instead, another transitional area from the isocortex side, called proisocortex, is formed at such borders. So, at borders between "true" archicortex and true isocortex, there are two transitional areas. One such area, which is anatomically located closer to the archicortex side and histologically more resembling it, is called periarchicortex. Another transitional area, which is anatomically located closer to the true isocortex and histologically more resembling it, is called proisocortex.


Memory cells (motor cortex)

Memory cells are found in the primary motor cortex (M1), a region located in the posterior portion of the frontal lobe of the brain. Their behavior is described by Bizzi et al. as:
For a quick review see
Also


Polynomial k-CFA


Gray ramus communicans

Each spinal nerve receives a branch called a gray ramus communicans (plural rami communicantes) from the adjacent paravertebral ganglion of the sympathetic trunk. The gray rami communicantes contain postganglionic nerve fibers of the sympathetic nervous system and are composed of largely unmyelinated neurons. This is in contrast to the white rami communicantes, in which heavily myelinated neurons give the rami their white appearance.
Function.
Preganglionic sympathetic fibres from the intermediolateral nucleus in the lateral grey column of the spinal cord are carried in the white ramus communicans to the paravertebral ganglia of the sympathetic trunk. Once the preganglionic nerve has traversed a white ramus communicans, it can do one of three things.
Ganglionic influence can be specifically targeted to end organs as well as becoming part of a summating systemic response. If the response is the whole body response, as in sympathetic fight or flight, the signals are distributed to other spinal nerves by way of gray rami communicantes which serve as conduits between the spinal nerves.


American Society of Appraisers

The American Society of Appraisers (ASA) is the largest multi-discipline, voluntary membership, trade association representing and promoting their member appraisers. The Society was founded in 1936 and is one of the eight trade association appraisal groups that founded The Appraisal Foundation.
In 2017, the Society merged with National Association of Independent Fee Appraisers (NAIFA), bringing total membership to over 5,500 members in 75 countries.
The Society comprises appraisal review and management, business valuation, gems and jewelry, machinery and technical specialties, personal property and real property. Candidates—who must have a low level four-year university degree or its equivalent—are eligible for the Accredited Senior Appraiser (ASA) designation after completing the following: five years of documented appraisal experience; testing in their field or specialty; the submission of two appraisal reports to the society's International Board of Examiners for review; successful completion of the Principles of Valuation education program; and successful completion of the 15-hour Uniform Standards of Professional Appraisal Practice (USPAP) course with examination. A lesser level of designation—Accredited Member or AM—requires only two years of documented appraisal experience in addition to all of the other requirements. Both of these designations are entry level. They do not rise to the equivalent of a Masters or Phd. in finance, business or economics, though they do provide an educational floor of knowledge in these subjects.
Unlike a Masters education in finance from an accredited university, which requires a once in a lifetime payment, trade associations like the American Society of Appraisers require annual membership dues. In addition, in order to sustain its business model and cash flows, Voluntary Member Appraisers in the Society subject themselves to arbitrary mandatory re-accreditation process every five years. To re-certify they must provide proof of professional growth through continuing education, participation in society activities, and the completion of updated USPAP courses. Publishing articles in professional journals and valuation or specialty-related speaking engagements also provide Society's appraisers with re-certification credit. In addition, the organization will from time to time fractionalize, create and sell new credentials, which are a repeat and repackaging of old courses and concepts for these credentials under a new name.


Pes hippocampi

The lower end of the hippocampus is enlarged, and presents two or three rounded elevations or digitations which give it a paw-like appearance, and hence it is named the pes hippocampi ("pes" meaning "foot") or pes hippocampi major


Hypokalemic periodic paralysis

Hypokalemic periodic paralysis (hypoKPP), also known as familial hypokalemic periodic paralysis (FHPP), is a rare, autosomal dominant channelopathy characterized by muscle weakness or paralysis when there is a fall in potassium levels in the blood. In individuals with this mutation, attacks sometimes begin in adolescence and most commonly occur with individual triggers such as rest after strenuous exercise (attacks during exercise are rare), high carbohydrate meals, meals with high sodium content, sudden changes in temperature, and even excitement, noise, flashing lights, cold temperatures and stress. Weakness may be mild and limited to certain muscle groups, or more severe full-body paralysis. During an attack, reflexes may be decreased or absent. Attacks may last for a few hours or persist for several days. Recovery is usually sudden when it occurs, due to release of potassium from swollen muscles as they recover. Some patients may fall into an abortive attack or develop chronic muscle weakness later in life.
Some people only develop symptoms of periodic paralysis due to hyperthyroidism (overactive thyroid). This entity is distinguished with thyroid function tests, and the diagnosis is instead called thyrotoxic periodic paralysis.
Genetics.
Mutations in the following genes can cause hypokalemic periodic paralysis:
An association with "KCNE3" (voltage-gated potassium channel) has also been described, but is currently disputed, and excluded from the disease definition in OMIM.
Action potentials from the central nervous system cause end-plate potentials at the NMJ which causes sodium ions to enter and depolarise the muscle cells. This depolarisation propagates to the T-tubules where it triggers the entry of calcium ions via Cav1.1 as well as from the sarcoplasmic reticulum through the associated ryanodine receptor RyR1. This causes contraction (tensing) of the muscle. Depolarisation of the motor end plate causes potassium ions to leave the muscle cells, repolarising the muscle and closing the calcium channels. Calcium is pumped away from the contractile apparatus and the muscle relaxes.
Mutations altering the usual structure and function of these channels therefore disrupts regulation of muscle contraction, leading to episodes of severe muscle weakness or paralysis. Mutations have been identified in arginine residues making up the voltage sensor of Nav1.4. This voltage sensor comprises the S4 alpha helix of each of the four transmembrane domains (I-IV) of the protein, and contains basic residues that only allow entry of the positive sodium ions at appropriate membrane voltages by blocking or opening the channel pore. In Cav1.1, mutations have also been found in domains II and IV. These mutations are loss-of-function, such that the channels cannot open normally.
In patients with mutations in SCN4A or CACNA1S, therefore, the channel has a reduced excitability and signals from the central nervous system are unable to depolarise the muscle. As a result, the muscle cannot contract efficiently (paralysis). The condition is hypokalemic (manifests when potassium is low; not "causing hypokalemia") because a low extracellular potassium ion concentration will cause the muscle to repolarise to the resting potential more quickly, so even if calcium conductance does occur it cannot be sustained. It becomes more difficult to reach the calcium threshold at which the muscle can contract, and even if this is reached then the muscle is more likely to relax. Because of this, the severity would be reduced if potassium ion concentrations are kept high.
Mutations in KCNJ2 lead to hypokalemic periodic paralysis with cardiac arrhythmias called Andersen–Tawil syndrome.
In contrast, hyperkalemic periodic paralysis refers to gain-of-function mutations in sodium channels that maintain muscle depolarisation and therefore are aggravated by high potassium ion concentrations.
This condition is inherited in an autosomal dominant pattern (but with a high proportion of sporadic cases), which means one copy of the altered gene in each cell is sufficient to cause the disorder.
Signs and symptoms.
Hypokalemic periodic paralysis is a condition that causes episodes of extreme muscle weakness typically beginning in childhood or adolescence. Most often, these episodes involve a temporary inability to move muscles in the arms and legs. Attacks cause severe weakness or paralysis that usually lasts from hours to days. Some people may have episodes almost every day, while others experience them weekly, monthly, or only rarely. Attacks can occur without warning or can be triggered by factors such as rest after exercise, a viral illness, or certain medications. Often, a large, carbohydrate-rich meal or vigorous exercise in the evening can trigger an attack upon waking the following morning. Although affected individuals usually regain their muscle strength between attacks, some develop persistent muscle weakness later in life.
Diagnosis.
Diagnosis can be achieved through a specialized form of electromyographic (EMG) testing called the long exercise test. This test measures the amplitude of a nerve response (called the Compound Muscle Action Potential or CMAP) for 40 to 50 minutes following a few minutes of exercise. In affected patients, there is a progressive fall in the amplitude of the potential. Besides the patient history or a report of serum potassium low normal or low during an attack, the long exercise test is the current standard for medical testing. Genetic diagnosis is often unreliable as only a few of the more common gene locations are tested, but even with more extensive testing 20–37% of people with a clinical diagnosis of hypokalemic periodic paralysis have no known mutation in the two known genes. Standard EMG testing cannot diagnose a patient unless they are in a full blown attack at the time of testing. Provoking an attack with exercise and diet then trying oral potassium can be diagnostic, but also dangerous as this form of PP has an alternate form known as hyperkalemic periodic paralysis. The symptoms are almost the same, but the treatment is different. The old glucose insulin challenge is dangerous and risky to the point of being life-threatening and should never be done when other options are so readily available. Factors known to trigger episodes are: stress, cold environment or hypothermia, carbohydrate load, infection, glucose infusion, metabolic alkalosis, alcohol, strenuous exercise, and steroids.
People with hypokalemic periodic paralysis are often misdiagnosed as having a conversion disorder or hysterical paralysis since the weakness is muscle-based and doesn't correspond to nerve or spinal root distributions. The tendency of people with hypokalemic periodic paralysis to get paralyzed when epinephrine is released in "fight or flight" situations further adds to the temptation to misdiagnose the disorder as psychiatric.
Treatment.
Treatment of hypokalemic periodic paralysis focuses on preventing further attacks and relieving acute symptoms. Avoiding carbohydrate-rich meals, strenuous exercise and other identified triggers, and taking acetazolamide or another carbonic anhydrase inhibitor, may help prevent attacks of weakness. Some patients also take potassium-sparing diuretics such as spironolactone to help maintain potassium levels.
Paralysis attacks can be managed by drinking one of various potassium salts dissolved in water (debate exists over which, if any one in particular, is best used, but potassium chloride and bicarbonate are common). Rapidly absorbed boluses of liquid potassium are generally needed to abort an attack, but some patients also find positive maintenance results with time-released potassium tablets. IV potassium is seldom justified unless the patient is unable to swallow. Daily potassium dosage may need to be much higher than for potassium replacement from simple hypokalemia: 100-150 mEqs of potassium is often needed to manage daily fluctuations in muscle strength and function.
Perioperatively, prevention includes avoiding neuromuscular blockade, avoid excessive hyperventilation, warm the patient, provide adequate hydration, avoid glucose infusions, do not give diuretics, and closely monitor the electrocardiogram for signs of hypokalemia. Normal saline is the preferred IV solution for patients with familial hypokalemic periodic paralysis. Glucose containing solutions may cause weakness. Additionally, the high chloride content can cause a mild acidosis which would be preferred over alkalosis.
Prognosis.
The prognosis for periodic paralysis varies. Overactivity, a diet that is not low in sodium and carbohydrates, or simply an unfortunate gene mutation can lead to a type of chronic, low level weakness called an "abortive attack," or to permanent muscle damage. Abortive attacks often respond to extra potassium, cutting carbohydrates, getting plenty of rest, increasing doses of medication and gentle daily exercise such as short walks. Permanent muscle weakness is just what it sounds like: Permanent, irreparable damage to the muscles and associated weakness. Vacuoles and tubular aggregates form in and destroy healthy muscle tissue. This type of damage can typically be observed via a muscle biopsy. Not even anabolic steroids can repair this type of muscular damage.
Life span is expected to be normal, but attacks can drop potassium to levels low enough to cause life-threatening breathing problems or heart arrhythmia. Patients often report muscle pain and cognitive problems during attacks. Migraines occur in up to 50% of all hypokalemic periodic paralysis patients and may include less common symptoms like phantom smells, sensitivity to light and sound or loss of words. Medical literatures states that muscle strength is normal between attacks, but patients often report that their baseline strength is in fact lower than that of healthy individuals.
Because there are dozens of possible gene mutations, some drugs and treatments that work fine for one patient will not work for another. For example, most patients do well on acetazolamide, but some don't. Some patients will do well with extra magnesium (the body's natural ion channel blocker) or fish oil, while these same nutrients will make other patients worse. Patients and caregivers should take extreme caution with all new drugs and treatment plans.
History.
In 1935 the Scottish physician Dr Mary Walker was the first to recognise the association between familial periodical paralysis and hypokalaemia. She also described the glucose challenge test used in diagnosing hypokalaemic periodic paralysis and the use of intravenous potassium in its treatment.


Cellular neuroscience

Cellular neuroscience is a branch of neuroscience concerned with the study of neurons at a cellular level. This includes morphology and physiological properties of single neurons. Several techniques such as intracellular recording, patch-clamp, and voltage-clamp technique, pharmacology, confocal imaging, molecular biology, two photon laser scanning microscopy and Ca2+ imaging have been used to study activity at the cellular level. Cellular neuroscience examines the various types of neurons, the functions of different neurons, the influence of neurons upon each other, and how neurons work together.
Neurons and glial cells.
Neurons are cells that are specialized to receive, propagate, and transmit electrochemical impulses. In the human brain alone, there are over eighty billion neurons. Neurons are diverse with respect to morphology and function. Thus, not all neurons correspond to the stereotypical motor neuron with dendrites and myelinated axons that conduct action potentials. Some neurons such as photoreceptor cells, for example, do not have myelinated axons that conduct action potentials. Other unipolar neurons found in invertebrates do not even have distinguishing processes such as dendrites. Moreover, the distinctions based on function between neurons and other cells such as cardiac and muscle cells are not helpful. Thus, the fundamental difference between a neuron and a nonneuronal cell is a matter of degree.
Another major class of cells found in the nervous system are glial cells. These cells are only recently beginning to receive attention from neurobiologists for being involved not just in nourishment and support of neurons, but also in modulating synapses. For example, Schwann cells, which are a type of glial cell found in the peripheral nervous system, modulate synaptic connections between presynaptic terminals of motor neuron endplates and muscle fibers at neuromuscular junctions.
Neuronal function.
One prominent characteristic of many neurons is excitability. Neurons generate electrical impulses or changes in voltage of two types: graded potentials and action potentials. Graded potentials occur when the membrane potential depolarizes and hyperpolarizes in a graded fashion relative to the amount of stimulus that is applied to the neuron. An action potential on the other hand is an all-or-none electrical impulse. Despite being slower than graded potentials, action potentials have the advantage of traveling long distances in axons with little or no decrement. Much of the current knowledge of action potentials comes from squid axon experiments by Sir Alan Lloyd Hodgkin and Sir Andrew Huxley.
Action potential.
The Hodgkin–Huxley model of an action potential in the squid giant axon has been the basis for much of the current understanding of the ionic bases of action potentials. Briefly, the model states that the generation of an action potential is determined by two ions: Na+ and K+. An action potential can be divided into several sequential phases: threshold, rising phase, falling phase, undershoot phase, and recovery. Following several local graded depolarizations of the membrane potential, the threshold of excitation is reached, voltage-gated sodium channels are activated, which leads to an influx of Na+ ions. As Na+ ions enter the cell, the membrane potential is further depolarized, and more voltage-gated sodium channels are activated. Such a process is also known as a positive feedback loop. As the rising phase reaches its peak, voltage-gated Na+ channels are inactivated whereas voltage-gated K+ channels are activated, resulting in a net outward movement of K+ ions, which re-polarizes the membrane potential towards the resting membrane potential. Repolarization of the membrane potential continues, resulting in an undershoot phase or absolute refractory period. The undershoot phase occurs because unlike voltage-gated sodium channels, voltage-gated potassium channels inactivate much more slowly. Nevertheless, as more voltage-gated K+ channels become inactivated, the membrane potential recovers to its normal resting steady state..
Structure and formation of synapses.
Neurons communicate with one another via synapses. Synapses are specialized junctions between two cells in close apposition to one another. In a synapse, the neuron that sends the signal is the presynaptic neuron and the target cell receives that signal is the postsynaptic neuron or cell. Synapses can be either electrical or chemical. Electrical synapses are characterized by the formation of gap junctions that allow ions and other organic compound to instantaneously pass from one cell to another. Chemical synapses are characterized by the presynaptic release of neurotransmitters that diffuse across a synaptic cleft to bind with postsynaptic receptors. A neurotransmitter is a chemical messenger that is synthesized within neurons themselves and released by these same neurons to communicate with their postsynaptic target cells. A receptor is a transmembrane protein molecule that a neurotransmitter or drug binds. Chemical synapses are slower than electrical synapses.
Neurotransmitter transporters, receptors, and signaling mechanisms.
After neurotransmitters are synthesized, they are packaged and stored in vesicles. These vesicles are pooled together in terminal boutons of the presynaptic neuron. When there is a change in voltage in the terminal bouton, voltage-gated calcium channels embedded in the membranes of these boutons become activated. These allow Ca2+ ions to diffuse through these channels and bind with synaptic vesicles within the terminal boutons. Once bounded with Ca2+, the vesicles dock and fuse with the presynaptic membrane, and release neurotransmitters into the synaptic cleft by a process known as exocytosis. The neurotransmitters then diffuse across the synaptic cleft and bind to postsynaptic receptors embedded on the postsynaptic membrane of another neuron. There are two families of receptors: ionotropic and metabotropic receptors. Ionotropic receptors are a combination of a receptor and an ion channel. When ionotropic receptors are activated, certain ion species such as Na+ to enter the postsynaptic neuron, which depolarizes the postsynaptic membrane. If more of the same type of postsynaptic receptors are activated, then more Na+ will enter the postsynaptic membrane and depolarize cell. Metabotropic receptors on the other hand activate second messenger cascade systems that result in the opening of ion channel located some place else on the same postsynaptic membrane. Although slower than ionotropic receptors that function as on-and-off switches, metabotropic receptors have the advantage of changing the cell's responsiveness to ions and other metabolites, examples being gamma amino-butyric acid (inhibitory transmitter), glutamic acid (excitatory transmitter), dopamine, norepinephrine, epinephrine, melanin, serotonin, melatonin, endorphins, dynorphins, nociceptin, and substance P.
Postsynaptic depolarizations can either transmit excitatory or inhibitory neurotransmitters. Those that release excitatory vesicles are referred to as excitatory postsynaptic potential (EPSP). Alternatively, inhibitory vesicles stimulate postsynaptic receptors such as to allow Cl− ions to enter the cell or K+ ions to leave the cell, which results in an inhibitory postsynaptic potential (IPSP). If the EPSP is dominant, the threshold of excitation in the postsynaptic neuron may be reached, resulting in the generation of an action potential in the neuron(s) in turn postsynaptic to it, propagating the signal.
Synaptic plasticity.
Synaptic plasticity is the process whereby strengths of synaptic connections are altered. For example, long-term changes in synaptic connection may result in more postsynaptic receptors being embedded in the postsynaptic membrane, resulting in the strengthening of the synapse. Synaptic plasticity is also found to be the neural mechanism that underlies learning and memory. The basic properties, activity and regulation of membrane currents, synaptic transmission and synaptic plasticity, neurotransmission, neuroregensis, synaptogenesis and ion channels of cells are a few other fields studied by cellular neuroscientists. Tissue, cellular and subcellular anatomy are studied to provide insight into mental retardation at the Mental Retardation Research Center MRRC Cellular Neuroscience Core. Journals such as "Frontiers in Cellular Neuroscience" and "Molecular and Cellular Neuroscience" are published regarding cellular neuroscientific topics.


Hindustani vocabulary

Hindustani, also known as Hindi-Urdu, like all Indo-Aryan languages, has a core base of Sanskrit-derived vocabulary, which it gained through Prakrit. As such the standardized registers of the Hindustani language (Hindi-Urdu) share a common vocabulary, especially on the colloquial level. However, in formal speech, Hindi tends to draw on Sanskrit, while Urdu turns to Persian and sometimes Arabic. This difference lies in the history of Hindustani, in which the "lingua franca" started to gain more Persian words in urban areas (such as Delhi, Lucknow and Hyderabad), under the Delhi Sultanate; this dialect came to be termed Urdu.
The original Hindi dialects continued to develop alongside Urdu and according to Professor Afroz Taj, "the distinction between Hindi and Urdu was chiefly a question of style. A poet could draw upon Urdu's lexical richness to create an aura of elegant sophistication, or could use the simple rustic vocabulary of dialect Hindi to evoke the folk life of the village. Somewhere in the middle lay the day to day language spoken by the great majority of people. This day to day language was often referred to by the all-encompassing term "Hindustani"." In Colonial India, Hindi-Urdu acquired vocabulary introduced by Christian missionaries from the Germanic and Romanic languages, e.g. "pādrī" (Devanagari: पादरी, Nastaleeq: پادری) from "padre", meaning pastor.
When describing the state of Hindi-Urdu under the British Raj, Professor Śekhara Bandyopādhyāẏa stated that "Truly speaking, Hindi and Urdu, spoken by a great majority of people in north India, were the same language written in two scripts; Hindi was written in Devanagari script and therefore had a greater sprinkling of Sanskrit words, while Urdu was written in Persian script and thus had more Persian and Arabic words in it. At the more colloquial level, however, the two languages were mutually intelligible." After the partition of India, political forces within India tried to further Sanskritize Hindi, while political forces in Pakistan campaigned to remove Prakit/Sanskrit derived words from Urdu and supplant them with Persian and Arabic words. Despite these government efforts, the film industry, Bollywood continues to release its films in the original Hindustani (Hindi-Urdu) language, easily understood and enjoyed by speakers of both registers; in addition, many of the same television channels are viewed across the border.
Linguistic classification.
Hindi (हिन्दी "Hindi") is one of the Indo-Aryan languages of the Indo-European language family. The core of Hindi vocabulary is thus etymologically Indo-European. However, centuries of borrowing has led to the adoption of a wide range of words with foreign origins.
Examples of borrowed words.
Due to centuries of contact with Europeans, Turkic peoples, Arabs, Persians, and East Asians, Hindi has absorbed countless words from foreign languages, often totally integrating these borrowings into the core vocabulary. The most common borrowings from foreign languages come from three different kinds of contact. Close contact with neighboring peoples facilitated the borrowing of words from other Indian languages, Chinese, Burmese, and several indigenous Austroasiatic languages of North India. After centuries of invasions from Persia and the Middle East, particularly under the Mughal Empire, numerous Turkish, Arabic, and Persian words were absorbed and fully integrated into the lexicon. Later, European colonialism brought words from Portuguese, French, Dutch, and most significantly English. Some very common borrowings are shown below.
Borrowings from the Colonial Era.
Portuguese (पुर्तगाली پرتگالی "Purtugālī").
Portuguese borrowings mostly describe household items, fruits, and religious concepts dealing with Catholicism:
"Household"
"Food"
"Religion"
"Other"
French (फ़्रान्सीसी فرانسیسی "Fransisi").
Only a handful of French borrowings are still used in Hindi today.
English (अंग्रेज़ी انگریزی "Aṅgrezī").
Most borrowed words of European origin in Hindi-Urdu were imported through English and involve civic and household concepts:
"Civic Life"
"Household"


Roof of fourth ventricle

The roof of fourth ventricle is the dorsal surface of the fourth ventricle.
It corresponds to the ventral surface of the cerebellum.
The upper portion of the roof is formed by the cerebellum.
The roof of ventricle is diamond shaped and can be divided into superior and inferior parts.
The superior part or cranial part is formed by superior cerebellar peduncles and superior medullary velum.


Cranial nerves

Cranial nerves are the nerves that emerge directly from the brain (including the brainstem), of which there are conventionally considered twelve pairs. Cranial nerves relay information between the brain and parts of the body, primarily to and from regions of the head and neck, including the special senses of vision, taste, smell, and hearing.
The cranial nerves emerge from the central nervous system above the level of the first vertebrae of the vertebral column. Each cranial nerve is paired and is present on both sides. There are conventionally twelve pairs of cranial nerves, which are described with Roman numerals I–XII. Some considered there to be thirteen pairs of cranial nerves, including cranial nerve zero. The numbering of the cranial nerves is based on the order in which they emerge from the brain and brainstem, from front to back.
The terminal nerves (0), olfactory nerves (I) and optic nerves (II) emerge from the cerebrum, and the remaining ten pairs arise from the brainstem, which is the lower part of the brain.
The cranial nerves are considered components of the peripheral nervous system (PNS), although on a structural level the olfactory (I), optic (II), and trigeminal (V) nerves are more accurately considered part of the central nervous system (CNS).
The cranial nerves are in contrast to spinal nerves, which emerge from segments of the spinal cord.
Anatomy.
Most typically, humans are considered to have twelve pairs of cranial nerves (I–XII), with the terminal nerve (0) more recently canonized. The nerves are: the olfactory nerve (I), the optic nerve (II), oculomotor nerve (III), trochlear nerve (IV), trigeminal nerve (V), abducens nerve (VI), facial nerve (VII), vestibulocochlear nerve (VIII), glossopharyngeal nerve (IX), vagus nerve (X), accessory nerve (XI), and the hypoglossal nerve (XII).
Terminology.
Cranial nerves are generally named according to their structure or function. For example, the olfactory nerve (I) supplies smell, and the facial nerve (VII) supplies the muscles of the face. Because Latin was the "lingua franca" of the study of anatomy when the nerves were first documented, recorded, and discussed, many nerves maintain Latin or Greek names, including the trochlear nerve (IV), named according to its structure, as it supplies a muscle that attaches to a pulley (). The trigeminal nerve (V) is named in accordance with its three components ( meaning triplets), and the vagus nerve (X) is named for its wandering course ().
Cranial nerves are numbered based on their position from front to back (rostral-caudal) of their position on the brain, as, when viewing the forebrain and brainstem from below, they are often visible in their numeric order. For example, the olfactory nerves (I) and optic nerves (II) arise from the base of the forebrain, and the other nerves, III to XII, arise from the brainstem.
Cranial nerves have paths within and outside the skull. The paths within the skull are called "intracranial" and the paths outside the skull are called "extracranial". There are many holes in the skull called "foramina" by which the nerves can exit the skull. All cranial nerves are "paired", which means they occur on both the right and left sides of the body. The muscle, skin, or additional function supplied by a nerve, on the same side of the body as the side it originates from, is an "ipsilateral" function. If the function is on the opposite side to the origin of the nerve, this is known as a "contralateral" function.
Intracranial course.
Nuclei.
Grossly, all cranial nerves have a nucleus. With the exception of the olfactory nerve (I) and optic nerve (II), all the nuclei are present in the brainstem.
The midbrain of the brainstem has the nuclei of the oculomotor nerve (III) and trochlear nerve (IV); the pons has the nuclei of the trigeminal nerve (V), abducens nerve (VI), facial nerve (VII) and vestibulocochlear nerve (VIII); and the medulla has the nuclei of the glossopharyngeal nerve (IX), vagus nerve (X), accessory nerve (XI) and hypoglossal nerve (XII). The olfactory nerve (I) emerges from the olfactory bulb, and depending slightly on division the optic nerve (II) is considered to emerge from the lateral geniculate nuclei.
Because each nerve may have several functions, the nerve fibres that make up the nerve may collect in more than one nucleus. For example, the trigeminal nerve (V), which has a sensory and a motor role, has at least four nuclei.
Exiting the brainstem.
With the exception of the olfactory nerve (I) and optic nerve (II), the cranial nerves emerge from the brainstem. The oculomotor nerve (III) and trochlear nerve (IV) emerge from the midbrain, the trigeminal (V), abducens (VI), facial (VII) and vestibulocochlea (VIII) from the pons, and the glossopharyngeal (IX), vagus (X), accessory (XI) and hypoglossal (XII) emerge from the medulla.
The olfactory nerve (I) and optic nerve (II) emerge separately. The olfactory nerves emerge from the olfactory bulbs on either side of the crista galli, a bony projection below the frontal lobe, and the optic nerves (II) emerge from the lateral colliculus, swellings on either side of the temporal lobes of the brain.
Ganglia.
The cranial nerves give rise to a number of ganglia, collections of the cell bodies of neurons in the nerves that are outside of the brain. These ganglia are both parasympathetic and sensory ganglia.
The sensory ganglia of the cranial nerves, directly correspond to the dorsal root ganglia of spinal nerves and are known as cranial nerve ganglia. Sensory ganglia exist for nerves with sensory function: V, VII, VIII, IX, X. There are also a number of parasympathetic cranial nerve ganglia. Sympathetic ganglia supplying the head and neck reside in the upper regions of the sympathetic trunk, and do not belong to the cranial nerves.
The ganglion of the sensory nerves, which are similar in structure to the dorsal root ganglion of the spinal cord, include:
Additional ganglia for nerves with parasympathetic function exist, and include the ciliary ganglion of the oculomotor nerve (III), the pterygopalatine ganglion of the maxillary nerve (V2), the submandibular ganglion of the lingual nerve, a branch of the facial nerve (VII), and the otic ganglion of the glossopharyngeal nerve (IX).
Exiting the skull and extracranial course.
After emerging from the brain, the cranial nerves travel within the skull, and some must leave it in order to reach their destinations. Often the nerves pass through holes in the skull, called foramina, as they travel to their destinations. Other nerves pass through bony canals, longer pathways enclosed by bone. These foramina and canals may contain more than one cranial nerve and may also contain blood vessels.
Development.
The cranial nerves are formed from the contribution of two specialized embryonic cell populations, cranial neural crest and ectodermal placodes. The components of the sensory nervous system of the head are derived from the neural crest and from an embryonic cell population developing in close proximity, the cranial sensory placodes (the olfactory, lens, otic, trigeminal, epibranchial and paratympanic placodes). The doble-origin cranial nerves are summarized in the following Table:
Contributions of neural crest cells and placodes to ganglia and cranial nerves
Abbreviations: CN, Cranial Nerve; m, purely motor nerve; mix, mixed nerve (sensory and motor); NC, neural crest; PA, pharyngeal (branchial) arch; r, rhombomere; s, purely sensory nerve. * There is no known ganglion of the accessory nerve. The cranial part of the accessory nerve sends occasional branches to the superior ganglion of the vagus nerve.
Function.
The cranial nerves provide motor and sensory supply mainly to the structures within the head and neck. The sensory supply includes both "general" sensation such as temperature and touch, and "special" senses such as taste, vision, smell, balance and hearing. The vagus nerve (X) provides sensory and autonomic (parasympathetic) supply to structures in the neck and also to most of the organs in the chest and abdomen.
Terminal nerve (0).
The terminal nerve (0) may not have a role in humans, although it has been implicated in hormonal responses to smell, sexual response and mate selection.
Smell (I).
The olfactory nerve (I) conveys information giving rise to the sense of smell.
Damage to the olfactory nerve (I) can cause an inability to smell (anosmia), a distortion in the sense of smell (parosmia), or a distortion or lack of taste.
Vision (II).
The optic nerve (II) transmits visual information.
Damage to the optic nerve (II) affects specific aspects of vision that depend on the location of the damage. A person may not be able to see objects on their left or right sides (homonymous hemianopsia), or may have difficulty seeing objects from their outer visual fields (bitemporal hemianopsia) if the optic chiasm is involved. Inflammation (optic neuritis) may impact the sharpness of vision or colour detection
Eye movement (III, IV, VI).
The oculomotor nerve (III), trochlear nerve (IV) and abducens nerve (VI) coordinate eye movement. The oculomotor nerve controls all muscles of the eye except for the superior oblique muscle controlled by the trochlear nerve (IV), and the lateral rectus muscle controlled by the abducens nerve (VI). This means the ability of the eye to look down and inwards is controlled by the trochlear nerve (IV), the ability to look outwards is controlled by the abducens nerve (VI), and all other movements are controlled by the oculomotor nerve (III)
Damage to these nerves may affect the movement of the eye. Damage may result in double vision (diplopia) because the movements of the eyes are not synchronized. Abnormalities of visual movement may also be seen on examination, such as jittering (nystagmus).
Damage to the oculomotor nerve (III) can cause double vision and inability to coordinate the movements of both eyes (strabismus), also eyelid drooping (ptosis) and pupil dilation (mydriasis). Lesions may also lead to inability to open the eye due to paralysis of the levator palpebrae muscle. Individuals suffering from a lesion to the oculomotor nerve may compensate by tilting their heads to alleviate symptoms due to paralysis of one or more of the eye muscles it controls.
Damage to the trochlear nerve (IV) can also cause double vision with the eye adducted and elevated. The result will be an eye which can not move downwards properly (especially downwards when in an inward position). This is due to impairment in the superior oblique muscle.
Damage to the abducens nerve (VI) can also result in double vision. This is due to impairment in the lateral rectus muscle, supplied by the abducens nerve.
Trigeminal nerve (V).
The trigeminal nerve (V) and its three main branches the ophthalmic (V1), maxillary (V2), and mandibular (V3) provide sensation to the skin of the face and also controls the muscles of chewing.
Damage to the trigeminal nerve leads to loss of sensation in an affected area. Other conditions affecting the trigeminal nerve (V) include trigeminal neuralgia, herpes zoster, sinusitis pain, presence of a dental abscess, and cluster headaches.
Facial expression (VII).
The facial nerve (VII) controls most muscles of facial expression, supplies the sensation of taste from the front two-thirds of the tongue, and controls the stapedius muscle. Most muscles are supplied by the cortex on the opposite side of the brain; the exception is the frontalis muscle of the forehead, in which the left and the right side of the muscle both receive inputs from both sides of the brain.
Damage to the facial nerve (VII) may cause facial palsy. This is where a person is unable to move the muscles on one or both sides of their face. The most common cause of this is Bell's palsy, the ultimate cause of which is unknown. Patients with Bell's palsy often have a drooping mouth on the affected side and often have trouble chewing because the buccinator muscle is affected. The facial nerve is also the most commonly affected cranial nerve in blunt trauma.
Hearing and balance (VIII).
The vestibulocochlear nerve (VIII) supplies information relating to balance and hearing via its two branches, the vestibular and cochlear nerves. The vestibular part is responsible for supplying sensation from the vestibules and semicircular canal of the inner ear, including information about balance, and is an important component of the vestibuloocular reflex, which keeps the head stable and allows the eyes to track moving objects. The cochlear nerve transmits information from the cochlea, allowing sound to be heard.
When damaged, the vestibular nerve may give rise to the sensation of spinning and dizziness (vertigo). Function of the vestibular nerve may be tested by putting cold and warm water in the ears and watching eye movements caloric stimulation. Damage to the vestibulocochlear nerve can also present as repetitive and involuntary eye movements (nystagmus), particularly when the eye is moving horizontally. Damage to the cochlear nerve will cause partial or complete deafness in the affected ear.
Oral sensation, taste, and salivation (IX).
The glossopharyngeal nerve (IX) supplies the stylopharyngeus muscle and provides sensation to the oropharynx and back of the tongue. The glossopharyngeal nerve also provides parasympathetic input to the parotid gland.
Damage to the nerve may cause failure of the gag reflex; a failure may also be seen in damage to the vagus nerve (X).
Vagus nerve (X).
The vagus nerve (X) provides sensory and parasympathetic supply to structures in the neck and also to most of the organs in the chest and abdomen.
Loss of function of the vagus nerve (X) will lead to a loss of parasympathetic supply to a very large number of structures. Major effects of damage to the vagus nerve may include a rise in blood pressure and heart rate. Isolated dysfunction of only the vagus nerve is rare, but - if the lesion is located above the point at which the vagus first branches off - can be indicated by a hoarse voice, due to dysfunction of one of its branches, the recurrent laryngeal nerve.
Damage to this nerve may result in difficulties swallowing.
Shoulder elevation and head-turning (XI).
The accessory nerve (XI) supplies the sternocleidomastoid and trapezius muscles.
Damage to the accessory nerve (XI) will lead to weakness in the trapezius muscle on the same side as the damage. The trapezius lifts the shoulder when shrugging, so the affected shoulder will not be able to shrug and the shoulder blade (scapula) will protrude into a winged position. Depending on the location of the lesion there may also be weakness present in the sternocleidomastoid muscle, which acts to turn the head so that the face points to the opposite side.
Tongue movement (XII).
The hypoglossal nerve (XII) supplies the intrinsic muscles of the tongue, controlling tongue movement. The hypoglossal nerve (XII) is unique in that it is supplied by the motor cortices of both hemispheres of the brain.
Damage to the nerve may lead to fasciculations or wasting (atrophy) of the muscles of the tongue. This will lead to weakness of tongue movement on that side. When damaged and extended, the tongue will move towards the weaker or damaged side, as shown in the image. The fasciculations of the tongue are sometimes said to look like a "bag of worms". Damage to the nerve tract or nucleus will not lead to atrophy or fasciculations, but only weakness of the muscles on the same side as the damage.
Clinical significance.
Examination.
Doctors, neurologists and other medical professionals may conduct a cranial nerve examination as part of a neurological examination to examine the cranial nerves. This is a highly formalised series of steps involving specific tests for each nerve. Dysfunction of a nerve identified during testing may point to a problem with the nerve or of a part of the brain.
A cranial nerve exam starts with observation of the patient, as some cranial nerve lesions may affect the symmetry of the eyes or face. Vision may be tested by examining the visual fields, or by examining the retina with an ophthalmoscope, using a process known as funduscopy. Visual field testing may be used to pin-point structural lesions in the optic nerve, or further along the visual pathways. Eye movement is tested and abnormalities such as nystagmus are observed for. The sensation of the face is tested, and patients are asked to perform different facial movements, such as puffing out of the cheeks. Hearing is checked by voice and tuning forks. The patient's uvula is examined. After performing a shrug and head turn, the patient's tongue function is assessed by various tongue movements.
Smell is not routinely tested, but if there is suspicion of a change in the sense of smell, each nostril is tested with substances of known odors such as coffee or soap. Intensely smelling substances, for example ammonia, may lead to the activation of pain receptors of the trigeminal nerve (V) located in the nasal cavity and this can confound olfactory testing.
Damage.
Compression.
Nerves may be compressed because of increased intracranial pressure, a mass effect of an intracerebral haemorrhage, or tumour that presses against the nerves and interferes with the transmission of impulses along the nerve. Loss of function of a cranial nerve may sometimes be the first symptom of an intracranial or skull base cancer.
An increase in intracranial pressure may lead to impairment of the optic nerves (II) due to compression of the surrounding veins and capillaries, causing swelling of the eyeball (papilloedema). A cancer, such as an optic glioma, may also impact the optic nerve (II). A pituitary tumour may compress the optic tracts or the optic chiasm of the optic nerve (II), leading to visual field loss. A pituitary tumour may also extend into the cavernous sinus, compressing the oculuomotor nerve (III), trochlear nerve (IV) and abducens nerve (VI), leading to double-vision and strabismus. These nerves may also be affected by herniation of the temporal lobes of the brain through the falx cerebri.
The cause of trigeminal neuralgia, in which one side of the face is exquisitely painful, is thought to be compression of the nerve by an artery as the nerve emerges from the brain stem. An acoustic neuroma, particularly at the junction between the pons and medulla, may compress the facial nerve (VII) and vestibulocochlear nerve (VIII), leading to hearing and sensory loss on the affected side.
Stroke.
Occlusion of blood vessels that supply the nerves or their nuclei, an ischemic stroke, may cause specific signs and symptoms relating to the damaged area. If there is a stroke of the midbrain, pons or medulla, various cranial nerves may be damaged, resulting in dysfunction and symptoms of . Thrombosis, such as a cavernous sinus thrombosis, refers to a clot (thrombus) affecting the venous drainage from the cavernous sinus, affects the optic (II), oculomotor (III), trochlear (IV), opthalamic branch of the trigeminal nerve (V1) and the abducens nerve (VI).
Inflammation.
Inflammation of a cranial nerve can occur as a result of infection, such as viral causes like reactivated herpes simplex virus, or can occur spontaneously. Inflammation of the facial nerve (VII) may result in Bell's palsy.
Multiple sclerosis, an inflammatory process resulting in a loss of the myelin sheathes which surround the cranial nerves, may cause a variety of shifting symptoms affecting multiple cranial nerves. Inflammation may also affect other cranial nerves. Other rarer inflammatory causes affecting the function of multiple cranial nerves include sarcoidosis, miliary tuberculosis, and inflammation of arteries, such as granulomatosis with polyangiitis.
Other.
Trauma to the skull, disease of bone, such as Paget's disease, and injury to nerves during surgery are other causes of nerve damage.
History.
The Graeco-Roman anatomist Galen (AD 129–210) named seven pairs of cranial nerves. Much later, in 1664, English anatomist Sir Thomas Willis suggested that there were actually 9 pairs of nerves. Finally, in 1778, German anatomist Samuel Soemmering named the 12 pairs of nerves that are generally accepted today. However, because many of the nerves emerge from the brain stem as rootlets, there is continual debate as to how many nerves there actually are, and how they should be grouped. For example, there is reason to consider both the olfactory (I) and optic (II) nerves to be brain tracts, rather than cranial nerves.
Other animals.
Cranial nerves are also present in other vertebrates. Other amniotes (non-amphibian tetrapods) have cranial nerves similar to those of humans. In anamniotes (fishes and amphibians), the accessory nerve (XI) and hypoglossal nerve (XII) do not exist, with the accessory nerve (XI) being an integral part of the vagus nerve (X); the hypoglossal nerve (XII) is represented by a variable number of spinal nerves emerging from vertebral segments fused into the occiput. These two nerves only became discrete nerves in the ancestors of amniotes (non-amphibian tetrapods). The very small terminal nerve (nerve N or O) exists in humans but may not be functional. In other animals, it appears to be important to sexual receptivity based on perceptions of pheromones.


Frankenfood


Rhombic lip

The rhombic lip is a posterior section of the developing metencephalon which can be recognized transiently within the vertebrate embryo. It extends posteriorly from the roof of the fourth ventricle to dorsal neuroepithelial cells. The rhombic lip can be divided into eight structural units based on rhombomeres 1-8 (r1-r8), which can be recognized at early stages of hindbrain development. Producing granule cells and five brainstem nuclei, the rhombic lip plays an important role in developing a complex cerebellar neural system.
History.
Through studies of human embryos performed in the late 1890s, Swiss anatomist Wilhelm His identified a portion of hindbrain neuroepithelium that was distinct from the rest of the hindbrain neuroepithelium in its morphology, sustained chromosomal division into late stages of embryogenesis, and deployment of streams of neurons through the hindbrain periphery. His named this zone "rautenlippe," or rhombic lip, because it seemed to emanate from the rhomboid-shaped opening of the fourth ventricle, much like the shape of a mouth. His proposed that the rhombic lip held the precerebellar precursors that would migrate ventrally to populate the pontine and olivary nuclei, but the methodologies available at the time limited the amount of evidence he could gather. The first real evidence that precerebellar neurons had a dorsal origin was obtained in the 1990s through the use of chick-quail chimeras, a technique in which portions of quail hindbrain neuroepithelium are grafted into chick embryos "in ovo". Tracking the ventral migration of the quail daughter cells confirmed His' theory.


Ganglionic eminence

The ganglionic eminence (GE) is a transitory structure in the development of the nervous system that guides cell and axon migration. It is present in the embryonic and fetal stages of neural development found between the thalamus and caudate nucleus.
The eminence is divided into three regions of the ventral ventricular zone of the telencephalon (a lateral, medial and caudal eminence), where they facilitate tangential cell migration during embryonic development. Tangential migration does not involve interactions with radial glial cells; instead the interneurons migrate perpendicularly through the radial glial cells to reach their final location. The characteristics and function of the cells that follow the tangential migration pathway seem to be closely related to the location and precise timing of their production, and the GEs contribute significantly to building up the GABAergic cortical cell population. Another structure that the GEs contribute to is the basal ganglia. The GEs also guide the axons growing from the thalamus into the cortex and vice versa.
In humans, the GEs disappear by one year of age. During development, neuronal migration continues until the extinction of the germ layer, at which point the remnants from the germ layer make up the eminences.
Categorization.
Ganglionic eminences are categorized into three groups based on their location within the subventricular zone:
A sulcus separates the medial and lateral ganglionic eminences. The expression of "Nkx2-1", "Gsx2", and "Pax6" is required to determine the independent progenitor cell populations in the LGE and MGE. Interactions between these three genes define the boundaries between the different progenitor zones and mutations of these genes can cause abnormal expansion around the MGE, LGE, ventral pallium (VP), and anterior entopeduncular region (AEP). The cells of the GEs are quite homogenous, with the MGE, LGE, and CGE all having small, dark, irregular nuclei and moderately dense cytoplasm, however, each eminence can be identified by the type of progeny that it produces. See the individual GE sections below for more information on the different types of progeny produced.
Additionally, the subventricular zone is the starting point of multiple streams of tangentially migrating interneurons that express "Dlx" genes. There are three main tangential migration pathways that have been identified in this region:
These pathways are temporally and spatially distinct, and produce a variety of GABAergic, and non-GABAergic
interneurons. One example of GABAergic interneurons that the GEs guide are parvalbumin-containing interneurons in the neocortex. Some examples of non-GABAergic interneurons that the GEs guide are dopaminergic interneurons in the olfactory bulb, and cholinergic interneurons in the striatum. Cells migrating along these pathways move at different rates. Some molecules that have been implicated in controlling the rate of the unidirectional movement of cells derived from the GEs are hepatocyte growth factor/scattered factor (HGF/SF), and various neurotrophic factors.
Medial ganglionic eminence (MGE).
The primary purpose of the MGE during development is to produce GABAergic stellate cells and direct their migration to the neocortex. The precursors of most GABAergic interneurons in the cerebral cortex migrate from the subcortical progenitor zone. More specifically, performing a mechanical transection of the migratory route from the MGE to the neocortex causes a 33% decrease in GABAergic interneurons in the neocortex. The MGE also produces some of the neurons and glia of the basal ganglia and hippocampus. The MGE may also be a source of Cajal-Retzius cells, but this remains controversial. Early in embryonic development, the interneurons in the cortex stem primarily from the MGE and the AEP. In vitro experiments show that MGE cells migrate more than 300 μm per day, three times faster than the migration of LGE cells. See more about the time frame and function of MGE in comparison to the LGE in the following section.
Lateral ganglionic eminence (LGE).
Compared to the early temporal frame of development in the MGE, the LGE aids in the tangential migration of cells later in the mid-embryogenic stage. Unlike the MGE, which guides most cell migration into the cortex during this stage, the LGE contributes less to cell migration to the cortex, and instead guides many cells to the olfactory bulbs. In fact, the migration to the olfactory bulb is led by the LGE into adulthood. The route that newly generated neurons take from the anterior subventricular zone to the olfactory bulb is called the rostral migratory stream. During the late stages of embryonic development, both the LGE and MGE guide cell migration to the cortex, specifically the proliferative regions of the cortex. Some studies have found that the LGE also contributes cells to the neocortex, but this remains an issue of debate. In vitro, cells migrating from the LGE travel at a rate of 100 μm per day, slower than the MGE cells.
Caudal ganglionic eminence (CGE).
The caudal ganglionic eminence is another subcortical structure that is essential to the generation of cortical interneurons. It is located next to the lateral ventricle, posterior to where the LGE and MGE fuse. The CGE is a fusion of the rostral medial and lateral ganglionic eminence, which begins at the mid to caudal thalamus. There are two molecular domains that exist within the CGE and closely resemble extensions of the caudal MGE and LGE. The CGE is distinct from the LGE and MGE in gene expression patterns and progeny produced. Unlike the cells from the MGE, the cells from the CGE were rarely parvalbumin-containing neurons. It seems that the majority of cells from the CGE were GABAergic interneurons, but depending on where they are located, CGE-derived cells are very diverse. CGE-derived cells include GABAergic interneurons, spiny interneurons, mossy cells, pyramidal and granule neurons, and even oligodendrocyte and astrocyte glial cells.
Cell migration.
Cells in the ganglionic eminence migrate tangentially to neocortex, giving rise to interneurons. A variety of molecular mechanisms cooperate to direct this process. Embryonic interneuronal migration to the cerebral cortex is mediated by an array of motogenic growth factors in the MGE, repulsive factors in the striatum and LGE, permissive factors in migratory corridors in the ganglionic eminence, and attractive factors in the cortex itself. Cells in the LGE migrate to the striatal domain (caudate nucleus and putamen) and parts of the septum and amygdala. MGE cells follow a migratory path to the globus pallidus and part of the septum. The CGE gives rise to interneurons in the nucleus accumbens, the bed nucleus of the stria terminals, the hippocampus, and specific nuclei in the amygdala. This directed migration is induced by differences in gene expression between these subpallial domains. An array of genes are involved in the differentiation and specification of interneurons and oligodendrocytes, including: "Dlx1", "Dlx2", "Gsh1", "Mash1", "Gsh2", "Nkx2.1", "Nkx5.1", "Isl1", "Six3" and "Vax1".
Molecular mechanisms for directed migration.
The induced migration of cells from the ganglionic eminence during development is directed by a variety of motogenic factors, molecules that increase cell motility, and chemotactic molecules. The motogenic factor HGF/SF enhances cell motility and directs cells away from subpallial regions and demarcates the routes followed by migrating cells. Neurotrophins, such as BDNF, are a family of motogenic factors involved in directing migration. The cerebral cortex provides chemoattractant molecules (for example NRG1 type I and II in the cortex) while subpallial areas produce chemorepulsive molecules (for example Slit) to direct cell migration. Additionally, some permissive factors (such as NRG1 type III) in the migratory corridors are necessary for this process to occur.
The neurotransmitters GABA and 5-HT have been implicated in the migration as well. High GABA concentrations have been seen to cause random cell movement ("random walk migration"), while low concentrations promote directed migration. 5-HT has been tied to the process of incorporating interneurons into the cortical plate, as well as in the differentiation into subpopulations of interneurons.
Associated disorders.
The migration of cells from the ventricular zone to their intended destination and the success of their differentiation can be interrupted in many different ways, including interference with mechanical motors or an alteration of molecular signals that initiate movement, lead the cell in migration, and terminate its migration. The function of the molecules that affect migration are not confined to cell movement, overlapping considerably with the events associated with neurogenesis. As a result, neuronal migration syndromes are difficult to classify. The largest class of neuronal migration syndromes is lissencephaly. This includes a spectrum of simplified cortex ranging from agyria (a total absence of cortical convolutions) to pachygyria (broadened gyri) with unusually thick cortex.
Mis-migration of neurons can also result in bilateral periventricular nodular heterotopia, a disease recognized by neuronal heterotopia lining the lateral ventricles. Zellweger Syndrome is characterized by a cortical dysplasia similar to polymicrogyria of cerebral and cerebellar cortex, occasionally with pachygyria surrounding the Sylvian fissure, and focal/subependymal heterotopia. Kallmann syndrome is recognized by anosmia associated with mental retardation, hypogonadism, and the failure of the olfactory bulb to develop.
Disorders of axonal projection and assembly are rarely pure, but closely related to neuronal migration genes. This notably includes agenesis of the corpus callosum.
Disturbances in the genesis of neural elements can result in cortical dysplasia. Examples include ectopic neurogenesis, microencephaly, and altered cell survival resulting in areas of hyperplasia, reduced apoptosis, and heterotopia.
Further research.
Further research could be done on the migration of cells from the basal ganglia to the neocortex. The molecular mechanisms in control of this are still not completely clarified. The number of known mutations that could interfere with neuronal migration is rapidly growing, and will continue to do so as further research is performed. The complexity of molecular steps needed to correctly place cells in a system as complicated as the brain is impressive, and as more pieces to this intricate puzzle arise, it will be easier to come up with strategies to remedy disorders associated with neuronal migration, and to potentially repair damage caused by trauma, stroke, maldevelopment, and aging.


Ventral posterior nucleus

The ventral posterior nucleus is the somato-sensory relay nucleus in thalamus of the brain.
Input and output.
The ventral posterior nucleus receives neuronal input from the medial lemniscus, spinothalamic tracts, and trigeminothalamic tract. It projects to the somatosensory cortex and the ascending reticuloactivation system.
Subdivisions.
The ventral posterior nucleus is divided into:
Function.
Functions in touch, body position, pain, temperature, itch, taste, and arousal. Modulates tremor in certain pathology.


Sievierodonetsk

Sievierodonetsk ( ), Sieverodonetsk ( ) or Severodonetsk ( ) is a city in the Luhansk Oblast of Ukraine. Sievierodonetsk has the status of a city of regional significance, It is located nearby the Seversky Donets River, approximately to the north north west from the Oblast capital, Luhansk. Sievierodonetsk is the acting administrative centre of Luhansk Oblast due to Luhansk being temporarily controlled by self-proclaimed "Luhansk People's Republic", which is beyond the control of the Government of Ukraine, similarly to Kramatorsk acting as the administrative center of Donetsk Oblast during the Russo-Ukrainian War - their previous cities are still "de jure" administrative centres. Its population is approximately .
Sievierodonetsk has several factories and a significant chemical production centre "Azot" (English translation: Nitrogen). There is a domestic airport in 6 km to the south from the city.
History.
The town appears on older maps as Donets (Donetz, Donez) after the river of the same name.
The foundation of modern Sievierodonetsk is closely connected with the beginning of construction of the Lysychansk Nitrogen Fertilizer Plant within the limits of the city of Lysychansk in 1934. Donets itself was already combined with Lysychansk. The first settlement of workers on the construction site was Liskhimstroi, near by Donets. In September 1935, the first school was opened in the settlement, a silicate brick plant started production, and the first three residential two-story houses were built. In 1940, there were 47 houses, a school, a club, a kindergarten, a nursery, and 10 buildings of a chemical combine in Liskhimstroi.
During the Second World War, Liskhimstroi was occupied by German troops on July 11, 1942. It was liberated by the Red Army on February 1, 1943. Work to restore and expand the Lysychansk Nitrogen Fertilizer Plant began on December 10, 1943. By 1946, the pre-war housing stock was completely restored, which amounted to 17,000 square meters.
In 1950, four variants of a new name for Liskhimstroi were proposed: Svetlograd, Komsomolsk-on-Donets, Mendeleevsk, and Sievierodonetsk. In the same year, Liskhimstroi was renamed Sievierodonetsk, after the Siverskyi Donets River, and received the status of an urban settlement. January 1, 1951, the chemical plant produced its first output of ammonium nitrate.
A local newspaper is published in the city since April 1965.
Events in 2014.
During the 2014 pro-Russian unrest in Ukraine the town was captured late May 2014 by pro-Russian militants. No Ukrainian presidential election in 2014 was held in the city as the militants did not allow the voting places to open and much of the Election commission property was either stolen or destroyed. On 22 July 2014, Ukrainian forces regained control of the city. Heavy fighting continued around the city for a number of days; on 23 July 2014 the National Guard of Ukraine and the Ukrainian Army had claimed to had freed the city from terrorists.
A bridge across Siverskyi Donets river was severely damaged during the war in 2014; it was re-opened in December 2016. The European Union contributed 93.8% of the funding for the restoration.
Demographics.
Ethnicity of the city's residents as of the 2001 census:
Sports.
The first Ukrainian championship in bandy was held in the city 19/2-2012. Azot Severodonetsk became champions.


Data-driven instruction

Data-driven instruction is an educational approach that relies on information to inform teaching and learning. The idea refers to a method teachers use to improve instruction by looking at the information they have about their students. It takes place within the classroom, compared to data-driven decision making. Data-driven instruction works on two levels. One, it provides teachers the ability to be more responsive to students’ needs, and two, it allows students to be in charge of their own learning. Data-driven instruction can be understood through examination of its history, how it is used in the classroom, its attributes, and examples from teachers using this process.
History.
Prior to the current emphasis on data and accountability in schools, some school leaders and education researchers focused on standards-based reform in education. From the idea of creating standards comes accountability, the idea that schools should report on their ability to meet the designated standards. Late in the last century and in the early 2000s, an increased emphasis on accountability in public organizations made its way into the realm of education. With the passing of the No Child Left Behind (NCLB) Act in 2001 came laws requiring schools to provide information to the public concerning the quality of education provided to students. To be able to provide such data, states were mandated to create accountability measures and yearly assessments to gauge the effectiveness of schools in meeting those measures. Following NCLB, more recent legislation under the Race to the Top Act further pushed states to use data gathering and reporting to demonstrate school’s ability to meet the demands of the public. Embedded in both NCLB and the Race to the Top Act is an assumption that the collection and use of data can lead to increased student performance.
Attributes.
Data in the classroom is any information that is visible during instruction that could be used to inform teaching and learning. Types of data include quantitative and qualitative data, although quantitative data is most often used for data-driven instruction. Examples of quantitative data include test scores, results on a quiz, and levels of performance on a periodic assessment. Examples of qualitative data include field notes, student work/artifacts, interviews, focus groups, digital pictures, video, reflective journals.
Quantitative and qualitative data is generally captured through two forms of assessments: formative and summative. Formative assessment is the information that is revealed and shared during instruction and is actionable by the teacher or student. Paul Black and Dylan Wiliam offer examples of classroom assessment that is formative in nature, including student observations and discussions, understand pupils’ needs and challenges, and looking at student work. Conversely, summative assessments are designed to determine whether or not a student can transfer their learning to new contexts, as well as for accountability purposes. Formative assessment is the use of information made evident during instruction in order to improve student progress and performance. Summative assessments occur after teaching and learning occurred.
Examples.
Understanding the differences between quantitative data vs. qualitative data, as well as formative assessment vs. summative assessment that tease out this data can be defined as assessment literacy. Building assessment literacy also includes knowing when to use which type of assessment and the resulting data to use to inform instruction. The purpose of data driven instruction is to use information to guide teaching and learning. Dylan Wiliam offers examples of data driven instruction using formative assessment:
Because of the lack of timely feedback regarding the results plus the inability to personalize the approach, summative assessments are not readily used for data driven instruction in the classroom. Instead, a variety of information gleaned from different forms of assessments should be used to make decisions about student progress and performance within data-driven instruction. The use of multiple measures of different forms and at different times to make instructional decisions is referred to as triangulation.
Data-Driven Instructional Systems.
Background and origins.
Data-Driven Instructional Systems refers to a comprehensive system of structures that school leaders and teachers design in order to incorporate the data into their instructions. Building on organizational and school change literature, Richard Halverson, Jeffrey Grigg, Reid Prichett, and Chris Thomas developed a DDIS framework in an attempt to describe how relevant actors manage school-level internal accountability to external accountability. Specifically, high-stakes external accountability policies such as No Child Left Behind Act (NCLB) was implemented to hold schools accountable for the reported standardized, summative assessment metrics. However, schools already had active internal accountability systems that place high emphasis on an ongoing cycle of instructional improvement based on the use of data including formative assessment results and behavioral information. Therefore, when the high-stakes accountability was implemented, schools naturally go through process of alignment between different types of data different purposes and the corresponding tension. Richard Halverson and his colleagues, employing case study approaches, explore leaders’ effort of coordination and alignment process which occurs between extant “central practices and cultures of schools” and “new accountability pressure” in a pursuit of improving student achievement score.
Key concepts.
In their article, Richard Halverson, Jeffrey Grigg, Reid Prichett, and Chris Thomas suggest that the DDIS framework is composed of six organizational functions: data acquisition; data reflection; program alignment; program design; formative feedback; test preparation.
Data Acquisition.
Data acquisition includes the data collection, data storage, and data reporting functions. “Data” in DDIS model is broadly conceptualized as any type of information that guides teaching and learning. In practice, schools collect academic data standardized assessment test scores, as well as non-academic data like student demographic information, community survey data, curricula, technological capacity, and behavioral records. In order to store such data, some schools develop their own local collection strategies using low-tech printouts and notebooks, whereas other schools rely on high-tech district storage systems, which provide tremendous amounts of reports. School leaders have discussions around which data needs to be reported and how to report the data in a way that they can use to guide teaching practices.
Data Reflection.
In the DDIS model, data reflection refers to collectively making sense of the reported data. District-level data retreats provide key opportunities for the schools within districts to identify the school-level strengths and weaknesses in terms of achievement data. Retreats help districts to develop district-level visions for instruction. In contrast, through local data reflection meetings, teachers have conversations focused on the individual students’ progress by examining each student’s performance on the assessed standards.
Program Alignment.
Richard Halverson and his colleagues states that program alignment function refers to “link[ing] the relevant content and performance standards with the actual content taught in classroom.” For example, the benchmark assessment results, as “problem-finding tools,” help educators to identify the curricular standards that are not aligned well with the current instructional programs.
Program Design.
After identifying the main areas in relation to students learning needs and school goals, leaders and teachers design interventions: faculty-based programs; curriculum-based programs; and student-based programs. In an effort to improve the faculty’s data literacy, educators are provided with a variety of professional development opportunities and coaching focused on professional interaction (faculty-based programs). In addition, educators modify their curriculum as a whole-classroom approach (curriculum-based programs) or develop customized instructional plans taking into account individual students’ needs (student-based programs).
Formative Feedback.
Educators interact with each other around the formative feedback on the local interventions implemented across classrooms and programs. Formative feedback systems are made of three main components: intervention, assessment, and actuation. Intervention artifacts here include curriculum materials like textbooks and experiments, or programs such as individualized education programs (Intervention). The effect of these intervention artifacts can be evaluated through formative assessments, either commercial or self-created, from the perspective that they had brought intended changes to teaching and learning (Assessment). In the actuation space, educators interpret the assessment results in relation to the initial goals of the intervention, and discuss how to modify the instruction delivery or assessment as measurement tools, which lays groundwork for the new interventions (Actuation).
Test Preparation.
This function is not intended for teachers to “teach to the test.” Rather, it points to the following activities: curriculum-embedded activities, test practice, environmental design, and community outreach. Teachers incorporate the content of standardized assessment into their day-to-day instructions (curriculum-embedded activities), assist students to practice or be accustomed to test-taking with similar types of tests (test practice), and establish a favorable test-taking environment (environmental design). Further, teachers communicate with parents and the community members on the topics ranging from test implementation to interpreting the test results (community outreach).
Implications.
For school districts.
The primary implication for school districts is in ensuring high quality and relevant data is gathered and available. Beyond creating systems to gather and share the data, the school district must provide the expertise, in the form of data expert personnel and/or the access to professional development resources to ensure school building leaders are able to access and use the data.
Another critical component of the responsibility of the district is to provide the leadership and vision to promulgate the use of information about student performance to improve teaching practice. Zavadsky and Dolejs suggest two areas for school districts to consider:
“The first is data collection and analysis. Districts and schools must carefully consider what data they need to collect, develop instruments with which to collect the data, and make the data available as soon as possible. The second component is data use. Principals and district leaders must give teachers sufficient time and training to understand the data and learn how to respond to what the data reveal”.
While the literature shows the vital importance of the role of the district in setting the stage for data driven instruction, more of the work of connecting student performance to classroom practices happens at the school and classroom level.
For schools.
Schools have a major role in establishing the conditions for data-driven instruction to flourish. Heppen, et al. indicate a need for a clear and consistent focus on using data and a data-rich environment to support teachers’ efforts to use data to drive instruction. When the leadership creates and maintains an environment which promotes collaboration and clearly communicates the urgency to improve student learning, teachers feel supported to engage in data use. The additional scaffold of modeling the use of data at the school level increases teachers’ expertise in the use of data.
For teachers.
Data-driven instruction is created and implemented in the classroom. Teachers have the most direct link between student performance and classroom practices. Through the use of data, teachers can make decisions about what and how to teach including how to use time in class, interventions for students who are not meeting standards, customizing lessons based on real-time information, adapting teaching practice to align to student needs, and making changes to pace, scope and sequence.
To be able to engage in data-driven instruction, teachers must first develop the knowledge, skills, and dispositions required. Working in a school culture and climate in which data-driven instruction is valued and supported, teachers have the ability to increase student achievement and potentially reduce the achievement gap. Additionally, teachers must have access to learning opportunities or professional development which helps them understand the pedagogical framework and technical skills required to obtain, analyze, and use information about students to make instructional decisions.
For students.
A significant new growth in data-driven instruction is in having students shape their lessons using data about their own progress. Younger learners who are able to self-report regarding grades and other assessments can experience high levels of achievement and progress within instruction. To embed data analysis by students into classroom practices, it requires time, training, and action. The strategies that students use to evaluate their own learning vary in effectiveness. In a meta-analysis, Dunlosky, Rawson, Marsh, Nathan & Willingham ranked ten learning strategies based on the projected impact each would have on achievement:
Highly Effective Strategies:
Moderately Effective Strategies:
Less Effective Strategies:
It is worth noting that the less effective strategies may be more commonly used in K-12 classrooms than the moderately effective and highly effective strategies. The authors suggest that students should be taught how to use more effective techniques and when they are most helpful in guiding their learning. When these strategies become internalized, students will have developed techniques in order to learn how to learn. This is critical as they move into the secondary level and are expected to be more independent in their studies.
Criticisms.
A major criticism of data driven instruction is that it focuses too much on test scores, and that not enough attention is given to the results of classroom assessments. Data driven instruction should serve as a “road map through assessment” that helps “teachers plan instruction to meet students’ needs, leading to better achievement”. Summative assessments should not be used to inform the day-to-day teaching and learning that is supported by data-driven instruction. Additional problems associated with perceptions of data driven instruction include the limitations of quantitative data to represent student learning, not considering the social and emotional needs or the context of the data when making instructional decisions, and a hyperfocus on the core areas of literacy and mathematics while ignoring the encore, traditionally high-interest areas such as the arts and humanities.