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#6004.
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M # 729.
Circumstances Quotes - VIII
1. The only sci-fi movie that I've ever been offered that, had circumstances been different, I would have definitely done, was 'Avatar.' And I literally couldn't do it because of my schedule. But listening to James Cameron talk about 'Avatar' was so fascinating. Because he literally invented the world in his mind - and it literally existed. - Matt Damon
2. Any use of chemical weapons, by anyone, under any circumstances, is a grave violation of the 1925 Protocol and other relevant rules of customary international law. - Ban Ki-moon
3. I think there were times when, if circumstances had developed, I might have been tempted into politics. I am a fan of Tony Blair. I think Gordon Brown is a fine man, but I think he's headed for one hell of a bloody struggle. - Richard Attenborough
4. I don't think people go to musicians for their political points of view. I think your political point of view is circumstances and then how you were nurtured and brought up. - Bruce Springsteen
5. I usually tried to stay in the net for 45 minutes, half an hour longer than most batsmen would stick at the county nets. There was a reason for this so-called gluttony of practice: it was a conscious effort to make myself concentrate for long periods of time in circumstances as close to the real thing as I could make them. - Geoffrey Boycott
6. I will never join politics under any circumstances. - Nana Patekar
7. The thing that always attracted me to New York was the sense of being in a place where a lot of people had a lot of stories not unlike mine. Everybody comes from somewhere else. Everyone's got a Polish grandmother, some kind of metamorphosis in their family circumstances. That's a very big thing - the experience of not living where you started. - Salman Rushdie.
Acetic Acid
Gist
Acetic acid is also known as ethanoic acid, ethylic acid, vinegar acid, and methane carboxylic acid. Acetic acid is a byproduct of fermentation, and gives vinegar its characteristic odor.
In the chemical industry, acetic acid is used in the production of cleaning products and, in the pharmaceutical industry, in supplements and some medicines, as it is capable of stabilising blood pressure and reducing blood sugar levels. It is also a common ingredient in ointments.
It is also used in some skin care products to adjust and maintain their pH. Acetic acid has antimicrobial properties – but not of the same potency or effectiveness as FDA-approved antimicrobial agents such as benzoyl peroxide.
Summary
Acetic acid is also known as ethanoic acid, ethylic acid, vinegar acid, and methane carboxylic acid. Acetic acid is a byproduct of fermentation, and gives vinegar its characteristic odor. Vinegar is about 4-6% acetic acid in water. More concentrated solutions can be found in laboratory use, and pure acetic acid containing only traces of water is known as glacial acetic acid. Dilute solutions like vinegar can contact skin with no harm, but more concentrated solutions will burn the skin. Glacial acetic acid can cause skin burns and permanent eye damage, and will corrode metal.
What is acetic acid used for?
Acetic acid is used in the manufacture of acetic anhydride, cellulose acetate, vinyl acetate monomer, acetic esters, chloracetic acid, plastics, dyes, insecticides, photographic chemicals, and rubber. Other commercial uses include the manufacture of vitamins, antibiotics, hormones, and organic chemicals, and as a food additive (acidulant). It is also used in various textile printing processes.
What are natural sources of acetic acid?
Acetates (salts of acetic acid) are common constituents of animal and plant tissues and are formed during the metabolism of food substances. Acetate is readily metabolized by most tissues and may give rise to the production of ketones as intermediates. Acetate is used by the body as a building block to make phospholipids, neutral lipids, steroids, sterols, and saturated and unsaturated fatty acids in a variety of human and animal tissue preparations.
What are the health effects of acetic acid exposure?
The low concentrations most people encounter in vinegar and other foods are harmless. At higher concentrations that could be encountered in a laboratory or factory, acetic acid is a strong eye, skin, and mucous membrane irritant. Prolonged skin contact with concentrated acetic acid may result in tissue destruction. Inhalation exposure to high concentrations of acetic acid vapors causes irritation of eyes, nose, and throat. People with high occupational exposure can develop conjunctivitis, bronchitis and pharyngitis, and erosion of exposed teeth (incisors and canines).
Details
Acetic acid, systematically named ethanoic acid, is an acidic, colourless liquid and organic compound with the chemical formula CH3COOH (also written as CH3CO2H, C2H4O2, or HC2H3O2). Vinegar is at least 4% acetic acid by volume, making acetic acid the main component of vinegar apart from water. It has been used, as a component of vinegar, throughout history from at least the third century BC.
Acetic acid is the second simplest carboxylic acid (after formic acid). It is an important chemical reagent and industrial chemical across various fields, used primarily in the production of cellulose acetate for photographic film, polyvinyl acetate for wood glue, and synthetic fibres and fabrics. In households, diluted acetic acid is often used in descaling agents. In the food industry, acetic acid is controlled by the food additive code E260 as an acidity regulator and as a condiment. In biochemistry, the acetyl group, derived from acetic acid, is fundamental to all forms of life. When bound to coenzyme A, it is central to the metabolism of carbohydrates and fats.
The global demand for acetic acid as of 2023 is about 17.88 million metric tonnes per year (t/a). Most of the world's acetic acid is produced via the carbonylation of methanol. Its production and subsequent industrial use poses health hazards to workers, including incidental skin damage and chronic respiratory injuries from inhalation.
Nomenclature
The trivial name "acetic acid" is the most commonly used and preferred IUPAC name. The systematic name "ethanoic acid", a valid IUPAC name, is constructed according to the substitutive nomenclature. The name "acetic acid" derives from the Latin word for vinegar, "acetum", which is related to the word "acid" itself.
"Glacial acetic acid" is a name for water-free (anhydrous) acetic acid. Similar to the German name "Eisessig" ("ice vinegar"), the name comes from the solid ice-like crystals that form with agitation, slightly below room temperature at 16.6 °C (61.9 °F). Acetic acid can never be truly water-free in an atmosphere that contains water, so the presence of 0.1% water in glacial acetic acid lowers its melting point by 0.2 °C.
A common symbol for acetic acid is AcOH (or HOAc), where Ac is the pseudoelement symbol representing the acetyl group CH3−C(=O)−; the conjugate base, acetate (CH3COO−), is thus represented as AcO−. Acetate is the ion resulting from loss of H+ from acetic acid. The name "acetate" can also refer to a salt containing this anion, or an ester of acetic acid. (The symbol Ac for the acetyl functional group is not to be confused with the symbol Ac for the element actinium; context prevents confusion among organic chemists). To better reflect its structure, acetic acid is often written as CH3−C(O)OH, CH3−C(=O)−OH, CH3COOH, and CH3CO2H. In the context of acid–base reactions, the abbreviation HAc is sometimes used, where Ac in this case is a symbol for acetate (rather than acetyl).
The carboxymethyl functional group derived from removing one hydrogen from the methyl group of acetic acid has the chemical formula −CH2−C(=O)−OH.
Additional Information
Acetic acid (CH3COOH) is the most important of the carboxylic acids. A dilute (approximately 5 percent by volume) solution of acetic acid produced by fermentation and oxidation of natural carbohydrates is called vinegar; a salt, ester, or acylal of acetic acid is called acetate. Industrially, acetic acid is used in the preparation of metal acetates, used in some printing processes; vinyl acetate, employed in the production of plastics; cellulose acetate, used in making photographic films and textiles; and volatile organic esters (such as ethyl and butyl acetates), widely used as solvents for resins, paints, and lacquers. Biologically, acetic acid is an important metabolic intermediate, and it occurs naturally in body fluids and in plant juices.
Acetic acid has been prepared on an industrial scale by air oxidation of acetaldehyde, by oxidation of ethanol (ethyl alcohol), and by oxidation of butane and butene. Today acetic acid is manufactured by a process developed by the chemical company Monsanto in the 1960s; it involves a rhodium-iodine catalyzed carbonylation of methanol (methyl alcohol).
2355) Hypotension
Gist
Low blood pressure is a condition in which the force of the blood pushing against the artery walls is too low. It's also called hypotension. Blood pressure is measured in millimeters of mercury (mm Hg). In general, low blood pressure is a reading lower than 90/60 mm Hg.
Low blood pressure occurs when blood pressure is much lower than normal. This means the heart, brain, and other parts of the body may not get enough blood. Normal blood pressure is mostly between 90/60 mmHg and 120/80 mmHg. The medical word for low blood pressure is hypotension.
Summary
Hypotension, also known as low blood pressure, is a cardiovascular condition characterized by abnormally reduced blood pressure. Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps out blood and is indicated by two numbers, the systolic blood pressure (the top number) and the diastolic blood pressure (the bottom number), which are the maximum and minimum blood pressures within the cardiac cycle, respectively. A systolic blood pressure of less than 90 millimeters of mercury (mmHg) or diastolic of less than 60 mmHg is generally considered to be hypotension. Different numbers apply to children. However, in practice, blood pressure is considered too low only if noticeable symptoms are present.
Symptoms may include dizziness, lightheadedness, confusion, feeling tired, weakness, headache, blurred vision, nausea, neck or back pain, an irregular heartbeat or feeling that the heart is skipping beats or fluttering, sweating, and fainting. Hypotension is the opposite of hypertension, which is high blood pressure. It is best understood as a physiological state rather than a disease. Severely low blood pressure can deprive the brain and other vital organs of oxygen and nutrients, leading to a life-threatening condition called shock. Shock is classified based on the underlying cause, including hypovolemic shock, cardiogenic shock, distributive shock, and obstructive shock.
Hypotension can be caused by strenuous exercise, excessive heat, low blood volume (hypovolemia), hormonal changes, widening of blood vessels, anemia, vitamin B12 deficiency, anaphylaxis, heart problems, or endocrine problems. Some medications can also lead to hypotension. There are also syndromes that can cause hypotension in patients including orthostatic hypotension, vasovagal syncope, and other rarer conditions.
For many people, excessively low blood pressure can cause dizziness and fainting or indicate serious heart, endocrine or neurological disorders.
For some people who exercise and are in top physical condition, low blood pressure could be normal. A single session of exercise can induce hypotension and water-based exercise can induce a hypotensive response.
Treatment depends on what causes low blood pressure. Treatment of hypotension may include the use of intravenous fluids or vasopressors. When using vasopressors, trying to achieve a mean arterial pressure (MAP) of greater than 70 mmHg does not appear to result in better outcomes than trying to achieve an MAP of greater than 65 mmHg in adults.
Details
Low blood pressure is a reading below 90/60 mm Hg. Many issues can cause low blood pressure. Treatment varies depending on what’s causing it. Symptoms of low blood pressure include dizziness and fainting, but many people don’t have symptoms. The cause also affects your prognosis.
Symptoms of low blood pressure include feeling tired or dizzy.
What is low blood pressure?
Hypotension, or low blood pressure, is when your blood pressure is much lower than expected. It can happen either as a condition on its own or as a symptom of a wide range of conditions. It may not cause symptoms. But when it does, you may need medical attention.
Types of low blood pressure
Hypotension has two definitions:
* Absolute hypotension: Your resting blood pressure is below 90/60 millimeters of mercury (mm Hg).
* Orthostatic hypotension: Your blood pressure stays low for longer than three minutes after you stand up from a sitting position. (It’s normal for your blood pressure to drop briefly when you change positions, but not for that long.) The drop must be 20 mm Hg or more for your systolic (top) pressure and 10 mm Hg or more for your diastolic (bottom) pressure. Another name for this is postural hypotension because it happens with changes in posture.
Measuring blood pressure involves two numbers:
Systolic (top number): This is the pressure on your arteries each time your heart beats.
Diastolic (bottom number): This is how much pressure your arteries are under between heartbeats.
What is considered low blood pressure?
Learn how blood pressure is measured.
Low blood pressure is below 90/60 mm Hg. Normal blood pressure is above that, up to 120/80 mm Hg.
How common is low blood pressure?
Because low blood pressure is common without any symptoms, it’s impossible to know how many people it affects. However, orthostatic hypotension seems to be more and more common as you get older. An estimated 5% of people have it at age 50, while that figure climbs to more than 30% in people over 70.
Who does low blood pressure affect?
Hypotension can affect people of any age and background, depending on why it happens. However, it’s more likely to cause symptoms in people over 50 (especially orthostatic hypotension). It can also happen (with no symptoms) to people who are very physically active, which is more common in younger people.
Symptoms and Causes:
What are the symptoms of low blood pressure?
Low blood pressure symptoms include:
* Dizziness or feeling lightheaded.
* Fainting or passing out (syncope).
* Nausea or vomiting.
* Distorted or blurred vision.
* Fast, shallow breathing.
* Fatigue or weakness.
* Feeling tired, sluggish or lethargic.
* Confusion or trouble concentrating.
* Agitation or other unusual changes in behavior (a person not acting like themselves).
For people with symptoms, the effects depend on why hypotension is happening, how fast it develops and what caused it. Slow decreases in blood pressure happen normally, so hypotension becomes more common as people get older. Fast decreases in blood pressure can mean certain parts of your body aren’t getting enough blood flow. That can have effects that are unpleasant, disruptive or even dangerous.
Usually, your body can automatically control your blood pressure and keep it from dropping too much. If it starts to drop, your body tries to make up for that, either by speeding up your heart rate or constricting blood vessels to make them narrower. Symptoms of hypotension happen when your body can’t offset the drop in blood pressure.
For many people, hypotension doesn’t cause any symptoms. Many people don’t even know their blood pressure is low unless they measure their blood pressure.
What are the possible signs of low blood pressure?
Your healthcare provider may observe these signs of low blood pressure:
* A heart rate that’s too slow or too fast.
* A skin color that looks lighter than it usually does.
* Cool kneecaps.
* Low cardiac output (how much blood your heart pumps).
* Low urine (pee) output.
What causes low blood pressure?
Hypotension can happen for a wide range of reasons. Causes of low blood pressure include:
* Orthostatic hypotension: This happens when you stand up too quickly and your body can’t compensate with more blood flow to your brain.
* Central nervous system diseases: Conditions like Parkinson’s disease can affect how your nervous system controls your blood pressure. People with these conditions may feel the effects of low blood pressure after eating because their digestive systems use more blood as they digest food.
* Low blood volume: Blood loss from severe injuries can cause low blood pressure. Dehydration can also contribute to low blood volume.
* Life-threatening conditions: These conditions include irregular heart rhythms (arrhythmias), pulmonary embolism (PE), heart attacks and collapsed lung. Life-threatening allergic reactions (anaphylaxis) or immune reactions to severe infections (sepsis) can also cause hypotension.
* Heart and lung conditions: You can get hypotension when your heart beats too quickly or too slowly, or if your lungs aren’t working as they should. Advanced heart failure (weak heart muscle) is another cause.
* Prescription medications: Hypotension can happen with medications that treat high blood pressure, heart failure, erectile dysfunction, neurological problems, depression and more. Don’t stop taking any prescribed medicine unless your provider tells you to stop.
* Alcohol or recreational drugs: Recreational drugs can lower your blood pressure, as can alcohol (for a short time). Certain herbal supplements, vitamins or home remedies can also lower your blood pressure. This is why you should always include these when you tell your healthcare provider what medications you’re taking.
* Pregnancy: Orthostatic hypotension is possible in the first and second trimesters of pregnancy. Bleeding or other complications of pregnancy can also cause low blood pressure.
* Extreme temperatures: Being too hot or too cold can affect hypotension and make its effects worse.
What are the complications of low blood pressure?
Complications that can happen because of hypotension include:
* Falls and fall-related injuries: These are the biggest risks with hypotension because it can cause dizziness and fainting. Falls can lead to broken bones, concussions and other serious or even life-threatening injuries. If you have hypotension, preventing falls should be one of your biggest priorities.
* Shock: When your blood pressure is low, that can affect your organs by reducing the amount of blood they get. That can cause organ damage or even shock (where your body starts to shut down because of limited blood flow and oxygen).
* Heart problems or stroke: Low blood pressure can cause your heart to try to compensate by pumping faster or harder. Over time, that can cause permanent heart damage and even heart failure. It can also cause problems like deep vein thrombosis (DVT) and stroke because blood isn’t flowing like it should, causing clots to form.
Diagnosis and Tests:
How is low blood pressure diagnosed?
Hypotension itself is easy to diagnose. Taking your blood pressure is all you need to do. But figuring out why you have hypotension is another story. If you have symptoms, a healthcare provider will likely use a variety of tests to figure out why it’s happening and if there’s any danger to you because of it.
What tests will be done to diagnose low blood pressure?
Your provider may recommend the following tests:
Lab testing
Tests on your blood and pee (urine) can look for any potential problems, like:
* Diabetes.
* Vitamin deficiencies.
* Thyroid or hormone problems.
* Low iron levels (anemia).
* Pregnancy (for anyone who can become pregnant).
Imaging
If providers suspect a heart or lung problem is behind your hypotension, they’ll likely use imaging tests to see if they’re right. These tests include:
* X-rays.
* Computed tomography (CT) scans.
* Magnetic resonance imaging (MRI).
* Echocardiogram or similar ultrasound-based tests.
Diagnostic testing
These tests look for specific problems with your heart or other body systems.
* Electrocardiogram (ECG or EKG).
* Exercise stress testing.
* Tilt table test (can help in diagnosing orthostatic hypotension).
Additional Information
Hypotension is a condition in which the blood pressure is abnormally low, either because of reduced blood volume or because of increased blood-vessel capacity. Though not in itself an indication of ill health, it often accompanies disease.
Extensive bleeding is an obvious cause of reduced blood volume that leads to hypotension. There are other possible causes. A person who has suffered an extensive burn loses blood plasma—blood minus the red and white blood cells and the platelets. Blood volume is reduced in a number of conditions involving loss of salt and water from the tissues—as in excessive sweating and diarrhea—and its replacement with water from the blood. Loss of water from the blood to the tissues may result from exposure to cold temperatures. Also, a person who remains standing for as long as one-half hour may temporarily lose as much as 15 percent of the blood water into the tissues of the legs.
Orthostatic hypotension—low blood pressure upon standing up—seems to stem from a failure in the autonomic nervous system. Normally, when a person stands up, there is a reflex constriction of the small arteries and veins to offset the effects of gravity. Hypotension from an increase in the capacity of the blood vessels is a factor in fainting (see syncope). Hypotension is also a factor in poliomyelitis, in shock, and in overdose of depressant drugs, such as barbiturates.
2158) John O'Keefe (neuroscientist)
Gist:
Life
John O'Keefe was born in New York City, and has dual US-British citizenship. He received a PhD in physiological psychology at McGill University in Montreal, Canada in 1967, and then moved to England to do research at University College London. He stayed in London and in 1987 was appointed professor of cognitive neuroscience at University College. John O'Keefe is currently director of the Sainsbury Wellcome Centre for Neural Circuits and Behaviour at University College.
Work
The awareness of one’s location and how to find the way to other places is crucial for both humans and animals. To understand the ability to orient ourselves in space, John O’Keefe studied the movements of rats and signals from nerve cells in the hippocampus, an area located in the center of the brain. In 1971 he discovered that when a rat was at a certain location in a room, certain cells were activated, and that when the rat moved to another location, other cells became activated. That is to say, the cells form a kind of internal map of the room.
Summary
John O’Keefe (born November 18, 1939, New York City, New York, U.S.) is a British-American neuroscientist who contributed to the discovery of place cells in the hippocampus of the brain and elucidated their role in cognitive (spatial) mapping. O’Keefe’s investigations of impairments in the cognitive mapping abilities of rats had important implications for the understanding of Alzheimer disease and other human neurological conditions in which affected persons fail to recognize their surroundings. For his contributions to the understanding of neural processes involved in the mental representation of spatial environments, O’Keefe shared the 2014 Nobel Prize for Physiology or Medicine with Norwegian neuroscientists May-Britt Moser and Edvard I. Moser.
O’Keefe grew up in New York City, the son of Irish immigrants. He studied aeronautical engineering at New York University before enrolling in 1960 at the City College of New York (CCNY) to study philosophy of the mind. After earning a bachelor’s degree from CCNY in 1963, he went to McGill University in Montreal, where he carried out graduate studies in the school’s psychology department. At McGill O’Keefe worked in the laboratory of Canadian psychologist Ronald Melzack, researching the sensory properties of the amygdala (a part of the brain involved in the fight-or-flight response) and developing tools and methods for his investigations. He completed a doctorate degree in physiological psychology in 1967, that same year joining University College London (UCL) as a postdoctoral research fellow. He remained at UCL for the duration of his career, eventually serving as a professor of cognitive neuroscience.
Within a few years at UCL, O’Keefe shifted his research from the amygdala to the hippocampus, attempting to understand its role in animal behaviour. Using techniques to record the activity of individual neurons in the rat hippocampus, he was able to observe the responses of single cells and correlate their activity to specific behaviours. Of particular interest to O’Keefe were rats that had sustained damage to the hippocampus, which produced significant changes in behaviour, such as reduced performance on spatial tasks and hyperactivity in new environments. After many experiments, O’Keefe discovered that cell activity in certain areas of the hippocampus was a function of place, with activity related specifically to where an animal was in its environment. The particular hippocampal areas involved (e.g., CA1) were densely occupied by pyramidal cells—cells that in the context of orientation and navigation became known as place cells. In 1971, with his student Jonathan O. Dostrovsky, O’Keefe published his findings, proposing in their seminal paper that behavioral deficits in animals with hippocampal damage stemmed from the loss of neural systems involved in cognitive mapping.
In 1978 O’Keefe and colleague Lynn Nadel published The Hippocampus as a Cognitive Map, describing in detail a theory that placed the cognitive map—the existence of which was first proposed in 1948 by American psychologist Edward C. Tolman—specifically in the hippocampus. The theory met with skepticism but later gained support through key discoveries by other researchers, including the Mosers’ discovery in 2005 of grid cells—cells located in a part of the brain known as the dorsocaudal medial entorhinal cortex (dMEC) that produce a system of coordinates by which animals determine their spatial position and navigate their environment. Subsequent research revealed that place cells and grid cells interact, with the activity of place cells likely derived from the formation of grids.
The neural system elucidated by O’Keefe and colleagues was described popularly as an “inner GPS.” O’Keefe’s research was crucial in that it provided the first experimental evidence for such a system and offered insight into the ability of animals, including humans, to orient themselves within an environment, to navigate from one place to another, and to remember spatial information. The loss of those abilities in humans is a hallmark of neurological disease, particularly Alzheimer disease, for which O’Keefe’s findings opened up new avenues of research. His work also fueled progress in scientists’ understanding of human cognition, especially aspects of memory.
In addition to the Nobel Prize, O’Keefe was the recipient of other prestigious awards, including the 2013 Louisa Gross Horwitz Prize (shared with the Mosers) and the 2014 Kavli Prize in Neuroscience (shared with Canadian neuropsychologist Brenda Milner and American neurologist Marcus Raichle). O’Keefe was elected a fellow of the Royal Society in 1992 and of the U.K. Academy of Medical Sciences in 1998.
Details
John O'Keefe (born November 18, 1939) is an American-British neuroscientist, psychologist and a professor at University College London.
O'Keefe discovered place cells in the hippocampus, and that they show a specific kind of temporal coding in the form of theta phase precession. He shared the Nobel Prize in Physiology or Medicine in 2014, together with May-Britt Moser and Edvard Moser; he has received several other awards.
Early life and education
Born in New York City to Irish immigrant parents, O'Keefe attended Regis High School (Manhattan) and received a BA degree from the City College of New York in 1963. Neither of his parents had completed elementary school in Ireland, but his father attained a high school degree in New York. He went on to study at McGill University in Montreal, Quebec, Canada, where he obtained an MA degree in 1964, and a PhD degree in Psychology in 1967, supervised by Ronald Melzack.
Career and research
O'Keefe went to University College London in 1967 as a US NIMH postdoctoral research fellow working with the late Patrick Wall. He has been there ever since and was promoted to Professor in 1987. At the behest of his collaborators Edvard Moser and May-Britt Moser he was appointed to a part-time professorial chair at the Norwegian University of Science and Technology in 2014.
Discovery of place cells
O’Keefe and his student Jonathan Dostrovsky discovered place cells by systematically analyzing the environmental factors influencing the firing properties of individual hippocampal neurons. His many publications on place cells have been highly cited. In addition, he published an influential book with Lynn Nadel, proposing the functional role of the hippocampus as a cognitive map for spatial memory function. In extensions of his work, place cells have been analyzed experimentally or simulated in models in hundreds of papers.
Discovery of theta phase precession
In further research on place cells, O’Keefe found evidence for a distinctive variation of temporal coding of information by the timing of action potentials in place cells, relative to an oscillatory EEG cycle known as the theta rhythm, as opposed to spike timing within a single cell. In a 1993 paper, he and Michael Recce demonstrated that place cells spike at different phases relative to theta rhythm oscillations in the local field potential of the hippocampus. As a rat enters the firing field of a place cell, the spiking starts at late phases of theta rhythm, and as the rat moves through the firing field, the spikes shift to earlier phases of the theta cycle. This effect has been replicated in numerous subsequent papers, providing evidence for the coding of sensory input by the timing of spikes. Numerous models have addressed the potential physiological mechanisms of theta phase precession.
Prediction and discovery of boundary vector cells
In a paper in 1996, O'Keefe and Neil Burgess presented data showing shifts in the position and size of place cell firing fields when the barriers defining the environment were shifted. In this and subsequent papers, they presented a model of this phenomenon predicting the existence of boundary vector cells that would respond at a specific distance from barriers in the environment. Several years later, this explicit theoretical prediction was supported by extensive experimental data demonstrating boundary cells with the predicted properties in the subiculum and the medial entorhinal cortex (where they are sometimes referred to as border cells).
Awards and honours
O'Keefe was elected a Fellow of the Royal Society (FRS) in 1992 and a Fellow of the Academy of Medical Sciences (FMedSci) in 1998. In addition, he received the Feldberg Foundation Prize in 2001 and the Grawemeyer Award in psychology in 2006 (with Lynn Nadel). In 2007, he received the British Neuroscience Association Award for Outstanding Contribution to British Neuroscience and in 2008 he received the Federation of European Neuroscience Societies European Journal of Neuroscience Award. Later in 2008, O'Keefe was awarded the Gruber Prize in Neuroscience. He was appointed as the inaugural director of the Sainsbury Wellcome Centre for Neural Circuits and Behaviour. In 2013 he received the Louisa Gross Horwitz Prize (with Edvard Moser and May-Britt Moser). In 2014, he was a co-recipient of the Kavli Prize awarded by the Norwegian Academy of Science and Letters with Brenda Milner and Marcus Raichle. In 2016 he was elected to the National Academy of Sciences. In 2019, he was admitted to the Royal Irish Academy as an honorary member.
O'Keefe was awarded the Nobel Prize in Physiology or Medicine 2014, with May-Britt Moser and Edvard Moser.
O'Keefe received an honorary Doctor of Science degree from University College Cork on December 15, 2014. In May 2015, he received one from The City College of New York, and in June of the same year, he was awarded one from McGill University, both his alma maters.
In 2014 he received the Kavli Prize in Neuroscience "for the discovery of specialized brain networks for memory and cognition", together with Brenda Milner and Marcus Raichle.
On March 10, 2015, O'Keefe was the guest on BBC Radio 4's The Life Scientific.
Hi,
#10237. Name the discoverer (December 26, 1838 – October 8, 1904), a German chemist who discovered the element germanium in 1886, solidifying Dmitri Mendeleev's theory of periodicity.
#10238. Name the French chemist (8 February 1777 – 27 September 1838) credited with first isolating iodine, making early photography possible.
Hi,
#5825. What does the verb (used with object) remonstrate mean?
#5826. What does the noun remorse mean?
Hi,
#2802. What does the medical term Osteogenesis imperfecta mean?
Hi,
#9486.
Hi,
#6003.
Q: What does Olaf eat for lunch?
A: Icebergers.
* * *
Q: How does officer Judy Hopps stay in shape?
A: She does a lot of Hare-obics.
* * *
Q: Where do Disney characters like to eat?
A: Mickey D's (Mcdonald's).
* * *
Q: Does Mr. Otterton listen to Gazelle?
A: Yes, he's a rabid fan.
* * *
Q: Why was Cinderella kicked off the soccer team?
A: Because she always ran away from the ball!
* * *
Hi,
2323.
.Hi,
2322.
Hi,
#9485.
Hi,
#6002.
Circumstances Quotes - VII
1. Many exceedingly rich men are unhappy, but many middling circumstances are fortunate. - Herodotus
2. In specific circumstances the period of aging decline can set in earlier in a particular organ than in the organism as a whole which, in a certain general or theoretical sense, is left a cripple or invalid. - Wilhelm Ostwald
3. No political event can be judged outside of the era and the circumstances in which it took place. - Fidel Castro
4. I cannot think of any circumstances in which a government can go to war without the support of parliament. - Tony Blair
5. Had we really succeeded therefore in altering the period of vibration, which Maxwell, as I have just noted, held to be impossible? Or was there some disturbing circumstances from one or more factors which distorted the result? - Pieter Zeeman
6. It has from the beginning been carried on with as much vigor and as great care of our trade as was consistent with our safety at home and with the circumstances we were in at the beginning of the war. - Robert Walpole
7. I think the French Open, in many ways, brought out a certain characteristic in me and in my game that was already there. Just the circumstances allowed for it to be able to show. - Michael Chang
8. When the euro was born, it was born in the wrong economic circumstances. - John Major.
2354) Hypertension
Gist
Hypertension (high blood pressure) is when the pressure in your blood vessels is too high (140/90 mmHg or higher). It is common but can be serious if not treated. People with high blood pressure may not feel symptoms. The only way to know is to get your blood pressure checked.
Summary
High blood pressure (also called hypertension) can lead to serious problems like heart attacks or strokes. But lifestyle changes and blood pressure medicines can help you stay healthy.
Check if you're at risk of high blood pressure
High blood pressure is very common, especially in older adults. There are usually no symptoms, so you may not realise you have it.
Things that increase your chances of having high blood pressure include:
* your age – you're more likely to get high blood pressure as you get older
* having close relatives with high blood pressure
* your ethnicity – you're at higher risk if you have a Black African, Black Caribbean or South Asian ethnic background
* having an unhealthy diet – especially a diet that's high in salt
* being overweight
* smoking
* drinking too much alcohol
* feeling stressed over a long period
Non-urgent advice:Get your blood pressure checked at a pharmacy or GP surgery if:
* you think you might have high blood pressure or might be at risk of having high blood pressure
* you're aged 40 or over and have not had your blood pressure checked for more than 5 years.
Some pharmacies may charge for a blood pressure check.
Some workplaces also offer blood pressure checks. Check with your employer.
Symptoms of high blood pressure
High blood pressure does not usually cause any symptoms.
Many people have it without realising it.
Rarely, high blood pressure can cause symptoms such as:
* headaches
* blurred vision
* chest pain
But the only way to find out if you have high blood pressure is to get your blood pressure checked.
Details
Hypertension, also known as high blood pressure, is a long-term medical condition in which the blood pressure in the arteries is persistently elevated. High blood pressure usually does not cause symptoms itself. It is, however, a major risk factor for stroke, coronary artery disease, heart failure, atrial fibrillation, peripheral arterial disease, vision loss, chronic kidney disease, and dementia. Hypertension is a major cause of premature death worldwide.
High blood pressure is classified as primary (essential) hypertension or secondary hypertension. About 90–95% of cases are primary, defined as high blood pressure due to nonspecific lifestyle and genetic factors. Lifestyle factors that increase the risk include excess salt in the diet, excess body weight, smoking, physical inactivity and alcohol use. The remaining 5–10% of cases are categorized as secondary hypertension, defined as high blood pressure due to a clearly identifiable cause, such as chronic kidney disease, narrowing of the kidney arteries, an endocrine disorder, or the use of birth control pills.
Blood pressure is classified by two measurements, the systolic (first number) and diastolic (second number) pressures. For most adults, normal blood pressure at rest is within the range of 100–140 millimeters mercury (mmHg) systolic and 60–90 mmHg diastolic. For most adults, high blood pressure is present if the resting blood pressure is persistently at or above 130/80 or 140/90 mmHg. Different numbers apply to children. Ambulatory blood pressure monitoring over a 24-hour period appears more accurate than office-based blood pressure measurement.
Lifestyle changes and medications can lower blood pressure and decrease the risk of health complications. Lifestyle changes include weight loss, physical exercise, decreased salt intake, reducing alcohol intake, and a healthy diet. If lifestyle changes are not sufficient, blood pressure medications are used. Up to three medications taken concurrently can control blood pressure in 90% of people. The treatment of moderately high arterial blood pressure (defined as >160/100 mmHg) with medications is associated with an improved life expectancy. The effect of treatment of blood pressure between 130/80 mmHg and 160/100 mmHg is less clear, with some reviews finding benefit and others finding unclear benefit. High blood pressure affects 33% of the population globally. About half of all people with high blood pressure do not know that they have it. In 2019, high blood pressure was believed to have been a factor in 19% of all deaths (10.4 million globally).
Signs and symptoms
Hypertension is rarely accompanied by symptoms. Half of all people with hypertension are unaware that they have it. Hypertension is usually identified as part of health screening or when seeking healthcare for an unrelated problem.
Some people with high blood pressure report headaches, as well as lightheadedness, vertigo, tinnitus (buzzing or hissing in the ears), altered vision or fainting episodes. These symptoms, however, might be related to associated anxiety rather than the high blood pressure itself.
Long-standing untreated hypertension can cause organ damage with signs such as changes in the optic fundus seen by ophthalmoscopy. The severity of hypertensive retinopathy correlates roughly with the duration or the severity of the hypertension. Other hypertension-caused organ damage include chronic kidney disease and thickening of the heart muscle.
Secondary hypertension
Secondary hypertension is hypertension due to an identifiable cause, and may result in certain specific additional signs and symptoms. For example, as well as causing high blood pressure, Cushing's syndrome frequently causes truncal obesity, glucose intolerance, moon face, a hump of fat behind the neck and shoulders (referred to as a buffalo hump), and purple abdominal stretch marks. Hyperthyroidism frequently causes weight loss with increased appetite, fast heart rate, bulging eyes, and tremor. Renal artery stenosis may be associated with a localized abdominal bruit to the left or right of the midline, or in both locations. Coarctation of the aorta frequently causes a decreased blood pressure in the lower extremities relative to the arms, or delayed or absent femoral arterial pulses. Pheochromocytoma may cause abrupt episodes of hypertension accompanied by headache, palpitations, pale appearance, and excessive sweating.
Hypertensive crisis
Severely elevated blood pressure (equal to or greater than a systolic 180 mmHg or diastolic of 120 mmHg) is referred to as a hypertensive crisis. Hypertensive crisis is categorized as either hypertensive urgency or hypertensive emergency, according to the absence or presence of end organ damage, respectively.
In hypertensive urgency, there is no evidence of end organ damage resulting from the elevated blood pressure. In these cases, oral medications are used to lower the BP gradually over 24 to 48 hours.
In hypertensive emergency, there is evidence of direct damage to one or more organs. The most affected organs include the brain, kidney, heart and lungs, producing symptoms which may include confusion, drowsiness, chest pain and breathlessness. In hypertensive emergency, the blood pressure must be reduced more rapidly to stop ongoing organ damage; however, there is a lack of randomized controlled trial evidence for this approach.
Pregnancy
Hypertension occurs in approximately 8–10% of pregnancies. Two blood pressure measurements six hours apart of greater than 140/90 mmHg are diagnostic of hypertension in pregnancy. High blood pressure in pregnancy can be classified as pre-existing hypertension, gestational hypertension, or pre-eclampsia. Women who have chronic hypertension before their pregnancy are at increased risk of complications such as premature birth, low birthweight or stillbirth. Women who have high blood pressure and had complications in their pregnancy have three times the risk of developing cardiovascular disease compared to women with normal blood pressure who had no complications in pregnancy.
Pre-eclampsia is a serious condition of the second half of pregnancy and following delivery characterised by increased blood pressure and the presence of protein in the urine. It occurs in about 5% of pregnancies and is responsible for approximately 16% of all maternal deaths globally. Pre-eclampsia also doubles the risk of death of the baby around the time of birth. Usually there are no symptoms in pre-eclampsia and it is detected by routine screening. When symptoms of pre-eclampsia occur the most common are headache, visual disturbance (often "flashing lights"), vomiting, pain over the stomach, and swelling. Pre-eclampsia can occasionally progress to a life-threatening condition called eclampsia, which is a hypertensive emergency and has several serious complications including vision loss, brain swelling, seizures, kidney failure, pulmonary edema, and disseminated intravascular coagulation (a blood clotting disorder).
In contrast, gestational hypertension is defined as new-onset hypertension during pregnancy without protein in the urine.
There have been significant findings on how exercising can help reduce the effects of hypertension just after one bout of exercise. Exercising can help reduce hypertension as well as pre-eclampsia and eclampsia.
The acute physiological responses include an increase in cardiac output (CO) of the individual (increased heart rate and stroke volume). This increase in CO can inadvertently maintain the amount of blood going into the muscles, improving functionality of the muscle later. Exercising can also improve systolic and diastolic blood pressure making it easier for blood to pump to the body. Through regular bouts of physical activity, blood pressure can reduce the incidence of hypertension.
Aerobic exercise has been shown to regulate blood pressure more effectively than resistance training. It is recommended to see the effects of exercising, that a person should aim for 5-7 days/ week of aerobic exercise. This type of exercise should have an intensity of light to moderate, utilizing ~85% of max heart rate (220-age). Aerobic has shown a decrease in SBP by 5-15mmHg, versus resistance training showing a decrease of only 3-5mmHg. Aerobic exercises such as jogging, rowing, dancing, or hiking can decrease SBP the greatest. The decrease in SBP can regulate the effect of hypertension ensuring the baby will not be harmed. Resistance training takes a toll on the cardiovascular system in untrained individuals, leading to a reluctance in prescription of resistance training for hypertensive reduction purposes.
Children
Failure to thrive, seizures, irritability, lack of energy, and difficulty in breathing can be associated with hypertension in newborns and young infants. In older infants and children, hypertension can cause headache, unexplained irritability, fatigue, failure to thrive, blurred vision, nosebleeds, and facial paralysis.
Causes:
Primary hypertension
Primary (also termed essential) hypertension results from a complex interaction of genes and environmental factors. More than 2000 common genetic variants with small effects on blood pressure have been identified in association with high blood pressure, as well as some rare genetic variants with large effects on blood pressure. There is also evidence that DNA methylation at multiple nearby CpG sites may link some sequence variation to blood pressure, possibly via effects on vascular or renal function.
Blood pressure rises with aging in societies with a western diet and lifestyle, and the risk of becoming hypertensive in later life is substantial in most such societies. Several environmental or lifestyle factors influence blood pressure. Reducing dietary salt intake lowers blood pressure; as does weight loss, exercise training, vegetarian diets, increased dietary potassium intake and high dietary calcium supplementation. Increasing alcohol intake is associated with higher blood pressure, but the possible roles of other factors such as caffeine consumption, and vitamin D deficiency are less clear. Average blood pressure is higher in the winter than in the summer.
Depression is associated with hypertension and loneliness is also a risk factor. Periodontal disease is also associated with high blood pressure. Chemical element As exposure through drinking water is associated with elevated blood pressure. Air pollution is associated with hypertension. Whether these associations are causal is unknown. Gout and elevated blood uric acid are associated with hypertension and evidence from genetic (Mendelian Randomization) studies and clinical trials indicate this relationship is likely to be causal. Insulin resistance, which is common in obesity and is a component of syndrome X (or metabolic syndrome), can cause hyperuricemia and gout and is also associated with elevated blood pressure.
Events in early life, such as low birth weight, maternal smoking, and lack of breastfeeding may be risk factors for adult essential hypertension, although strength of the relationships is weak and the mechanisms linking these exposures to adult hypertension remain unclear.
Secondary hypertension
Secondary hypertension results from an identifiable cause. Kidney disease is the most common secondary cause of hypertension. Hypertension can also be caused by endocrine conditions, such as Cushing's syndrome, hyperthyroidism, hypothyroidism, acromegaly, Conn's syndrome or hyperaldosteronism, renal artery stenosis (from atherosclerosis or fibromuscular dysplasia), hyperparathyroidism, and pheochromocytoma. Other causes of secondary hypertension include obesity, sleep apnea, pregnancy, coarctation of the aorta, excessive eating of liquorice, excessive drinking of alcohol, certain prescription medicines, herbal remedies, and stimulants such as cocaine and methamphetamine.
A 2018 review found that any alcohol increased blood pressure in males while over one or two drinks increased the risk in females.
Additional Information
Hypertension is a condition that arises when the blood pressure is abnormally high. Hypertension occurs when the body’s smaller blood vessels (the arterioles) narrow, causing the blood to exert excessive pressure against the vessel walls and forcing the heart to work harder to maintain the pressure. Although the heart and blood vessels can tolerate increased blood pressure for months and even years, eventually the heart may enlarge (a condition called hypertrophy) and be weakened to the point of failure. Injury to blood vessels in the kidneys, brain, and eyes also may occur.
Blood pressure is actually a measure of two pressures, the systolic and the diastolic. The systolic pressure (the higher pressure and the first number recorded) is the force that blood exerts on the artery walls as the heart contracts to pump the blood to the peripheral organs and tissues. The diastolic pressure (the lower pressure and the second number recorded) is residual pressure exerted on the arteries as the heart relaxes between beats. A diagnosis of hypertension is made when blood pressure reaches or exceeds 140/90 mmHg (read as “140 over 90 millimeters of mercury”).
Classification
When there is no demonstrable underlying cause of hypertension, the condition is classified as essential hypertension. (Essential hypertension is also called primary or idiopathic hypertension.) This is by far the most common type of high blood pressure, occurring in 90 to 95 percent of patients. Genetic factors appear to play a major role in the occurrence of essential hypertension. Secondary hypertension is associated with an underlying disease, which may be renal, neurologic, or endocrine in origin; examples of such diseases include Bright disease (glomerulonephritis; inflammation of the urine-producing structures in the kidney), atherosclerosis of blood vessels in the brain, and Cushing syndrome (hyperactivity of the adrenal glands). In cases of secondary hypertension, correction of the underlying cause may cure the hypertension. Various external agents also can raise blood pressure. These include cocaine, amphetamines, cold remedies, thyroid supplements, corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs), and oral contraceptives.
Malignant hypertension is present when there is a sustained or sudden rise in diastolic blood pressure exceeding 120 mmHg, with accompanying evidence of damage to organs such as the eyes, brain, heart, and kidneys. Malignant hypertension is a medical emergency and requires immediate therapy and hospitalization.
Epidemiology
Elevated arterial pressure is one of the most important public health problems in developed countries. In the United States, for instance, nearly 30 percent of the adult population is hypertensive. High blood pressure is significantly more prevalent and serious among African Americans. Age, race, gender, smoking, alcohol intake, elevated serum cholesterol, salt intake, glucose intolerance, obesity, and stress all may contribute to the degree and prognosis of the disease. In both men and women, the risk of developing high blood pressure increases with age.
Hypertension has been called the “silent killer” because it usually produces no symptoms. It is important, therefore, for anyone with risk factors to have their blood pressure checked regularly and to make appropriate lifestyle changes.
Complications
The most common immediate cause of hypertension-related death is heart disease, but death from stroke or renal (kidney) failure is also frequent. Complications result directly from the increased pressure (cerebral hemorrhage, retinopathy, left ventricular hypertrophy, congestive heart failure, arterial aneurysm, and vascular rupture), from atherosclerosis (increased coronary, cerebral, and renal vascular resistance), and from decreased blood flow and ischemia (myocardial infarction, cerebral thrombosis and infarction, and renal nephrosclerosis). The risk of developing many of these complications is greatly elevated when hypertension is diagnosed in young adulthood.
Treatment
Effective treatment will reduce overall cardiovascular morbidity and mortality. Nondrug therapy consists of: (1) relief of stress, (2) dietary management (restricted intake of salt, calories, cholesterol, and saturated fats; sufficient intake of potassium, magnesium, calcium, and vitamin C), (3) regular aerobic exercise, (4) weight reduction, (5) smoking cessation, and (6) reduced intake of alcohol and caffeine.
Mild to moderate hypertension may be controlled by a single-drug regimen, although more severe cases often require a combination of two or more drugs. Diuretics are a common medication; these agents lower blood pressure primarily by reducing body fluids and thereby reducing peripheral resistance to blood flow. However, they deplete the body’s supply of potassium, so it is recommended that potassium supplements be added or that potassium-sparing diuretics be used. Beta-adrenergic blockers (beta-blockers) block the effects of epinephrine (adrenaline), thus easing the heart’s pumping action and widening blood vessels. Vasodilators act by relaxing smooth muscle in the walls of blood vessels, allowing small arteries to dilate and thereby decreasing total peripheral resistance. Calcium channel blockers promote peripheral vasodilation and reduce vascular resistance. Angiotensin-converting enzyme (ACE) inhibitors inhibit the generation of a potent vasoconstriction agent (angiotensin II), and they also may retard the degradation of a potent vasodilator (bradykinin) and involve the synthesis of vasodilatory prostaglandins. Angiotensin receptor antagonists are similar to ACE inhibitors in utility and tolerability, but instead of blocking the production of angiotensin II, they completely inhibit its binding to the angiotensin II receptor. Statins, best known for their use as cholesterol-lowering agents, have shown promise as antihypertensive drugs because of their ability to lower both diastolic and systolic blood pressure. The mechanism by which statins act to reduce blood pressure is unknown; however, scientists suspect that these drugs activate substances involved in vasodilation.
Other agents that may be used in the treatment of hypertension include the antidiabetic drug semaglutide and the drug aprocitentan. Semaglutide is used specifically in patients who are obese or overweight. The drug acts as a glucagon-like peptide-1 (GLP-1) receptor agonist; GLP-1 interacts with receptors in the brain involved in the regulation of appetite, and thus semaglutide effectively triggers a reduction in appetite and thereby helps relieve symptoms of weight-related complications, such as hypertension. Aprocitentan acts as an inhibitor at endothelin A and endothelin B receptors, preventing binding by endothelin-1, which is a key protein involved in the activation of vasoconstriction and inflammatory processes in blood vessels.
Coagulation
Gist
Blood clotting, or coagulation, is an important process that prevents excessive bleeding when a blood vessel is injured. Platelets (a type of blood cell) and proteins in your plasma (the liquid part of blood) work together to stop the bleeding by forming a clot over the injury.
Coagulation treatment is usually carried out before sedimentation and filtration. During the process, a coagulant is added to water, and its positive charge neutralizes the negative charge of suspended contaminants.
Coagulation consists of three pathways, the extrinsic, intrinsic, and common pathways, that interact together to form a stable blood clot. The extrinsic and intrinsic coagulation pathways both lead into the final common pathway by independently activating factor X.
Summary
Coagulation, in physiology, is the process by which a blood clot is formed. The formation of a clot is often referred to as secondary hemostasis, because it forms the second stage in the process of arresting the loss of blood from a ruptured vessel. The first stage, primary hemostasis, is characterized by blood vessel constriction (vasoconstriction) and platelet aggregation at the site of vessel injury. Under abnormal circumstances, clots can also form in a vessel that has not been breached; such clots can result in the occlusion (blockage) of the vessel.
Clotting is a sequential process that involves the interaction of numerous blood components called coagulation factors. There are 13 principal coagulation factors in all, and each of these has been assigned a Roman numeral, I to XIII. Coagulation can be initiated through the activation of two separate pathways, designated extrinsic and intrinsic. Both pathways result in the production of factor X. The activation of this factor marks the beginning of the so-called common pathway of coagulation, which results in the formation of a clot.
The extrinsic pathway is generally the first pathway activated in the coagulation process and is stimulated in response to a protein called tissue factor, which is expressed by cells that are normally found external to blood vessels. However, when a blood vessel breaks and these cells come into contact with blood, tissue factor activates factor VII, forming factor VIIa, which triggers a cascade of reactions that result in the rapid production of factor X. In contrast, the intrinsic pathway is activated by injury that occurs within a blood vessel. This pathway begins with the activation of factor XII (Hageman factor), which occurs when blood circulates over injured internal surfaces of vessels. Components of the intrinsic pathway also may be activated by the extrinsic pathway; for example, in addition to activating factor X, factor VIIa activates factor IX, a necessary component of the intrinsic pathway. Such cross-activation serves to amplify the coagulation process.
The production of factor X results in the cleavage of prothrombin (factor II) to thrombin (factor IIa). Thrombin, in turn, catalyzes the conversion of fibrinogen (factor I)—a soluble plasma protein—into long, sticky threads of insoluble fibrin (factor Ia). The fibrin threads form a mesh that traps platelets, blood cells, and plasma. Within minutes, the fibrin meshwork begins to contract, squeezing out its fluid contents. This process, called clot retraction, is the final step in coagulation. It yields a resilient, insoluble clot that can withstand the friction of blood flow.
Details
Coagulation, also known as clotting, is the process by which blood changes from a liquid to a gel, forming a blood clot. It results in hemostasis, the cessation of blood loss from a damaged vessel, followed by repair. The process of coagulation involves activation, adhesion and aggregation of platelets, as well as deposition and maturation of fibrin.
Coagulation begins almost instantly after an injury to the endothelium that lines a blood vessel. Exposure of blood to the subendothelial space initiates two processes: changes in platelets, and the exposure of subendothelial platelet tissue factor to coagulation factor VII, which ultimately leads to cross-linked fibrin formation. Platelets immediately form a plug at the site of injury; this is called primary hemostasis. Secondary hemostasis occurs simultaneously: additional coagulation factors beyond factor VII (listed below) respond in a cascade to form fibrin strands, which strengthen the platelet plug.
Coagulation is highly conserved throughout biology. In all mammals, coagulation involves both cellular components (platelets) and proteinaceous components (coagulation or clotting factors). The pathway in humans has been the most extensively researched and is the best understood. Disorders of coagulation can result in problems with hemorrhage, bruising, or thrombosis.
Role in disease
Coagulation defects may cause hemorrhage or thrombosis, and occasionally both, depending on the nature of the defect.
Platelet disorders
Platelet disorders are either congenital or acquired. Examples of congenital platelet disorders are Glanzmann's thrombasthenia, Bernard–Soulier syndrome (abnormal glycoprotein Ib-IX-V complex), gray platelet syndrome (deficient alpha granules), and delta storage pool deficiency (deficient dense granules). Most are rare. They predispose to hemorrhage. Von Willebrand disease is due to deficiency or abnormal function of von Willebrand factor, and leads to a similar bleeding pattern; its milder forms are relatively common.
Decreased platelet numbers (thrombocytopenia) is due to insufficient production (e.g., myelodysplastic syndrome or other bone marrow disorders), destruction by the immune system (immune thrombocytopenic purpura), or consumption (e.g., thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome, paroxysmal nocturnal hemoglobinuria, disseminated intravascular coagulation, heparin-induced thrombocytopenia). An increase in platelet count is called thrombocytosis, which may lead to formation of thromboembolisms; however, thrombocytosis may be associated with increased risk of either thrombosis or hemorrhage in patients with myeloproliferative neoplasm.
Coagulation factor disorders
The best-known coagulation factor disorders are the hemophilias. The three main forms are hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency or "Christmas disease") and hemophilia C (factor XI deficiency, mild bleeding tendency).
Von Willebrand disease (which behaves more like a platelet disorder except in severe cases), is the most common hereditary bleeding disorder and is characterized as being inherited autosomal recessive or dominant. In this disease, there is a defect in von Willebrand factor (vWF), which mediates the binding of glycoprotein Ib (GPIb) to collagen. This binding helps mediate the activation of platelets and formation of primary hemostasis.
In acute or chronic liver failure, there is insufficient production of coagulation factors, possibly increasing risk of bleeding during surgery.
Thrombosis is the pathological development of blood clots. These clots may break free and become mobile, forming an embolus or grow to such a size that occludes the vessel in which it developed. An embolism is said to occur when the thrombus (blood clot) becomes a mobile embolus and migrates to another part of the body, interfering with blood circulation and hence impairing organ function downstream of the occlusion. This causes ischemia and often leads to ischemic necrosis of tissue. Most cases of venous thrombosis are due to acquired states (older age, surgery, cancer, immobility). Unprovoked venous thrombosis may be related to inherited thrombophilias (e.g., factor V Leiden, antithrombin deficiency, and various other genetic deficiencies or variants), particularly in younger patients with family history of thrombosis; however, thrombotic events are more likely when acquired risk factors are superimposed on the inherited state.
Pharmacology:
Procoagulants
The use of adsorbent chemicals, such as zeolites, and other hemostatic agents are also used for sealing severe injuries quickly (such as in traumatic bleeding secondary to gunshot wounds). Thrombin and fibrin glue are used surgically to treat bleeding and to thrombose aneurysms. Hemostatic Powder Spray TC-325 is used to treated gastrointestinal bleeding.
Desmopressin is used to improve platelet function by activating arginine vasopressin receptor 1A.
Coagulation factor concentrates are used to treat hemophilia, to reverse the effects of anticoagulants, and to treat bleeding in people with impaired coagulation factor synthesis or increased consumption. Prothrombin complex concentrate, cryoprecipitate and fresh frozen plasma are commonly used coagulation factor products. Recombinant activated human factor VII is sometimes used in the treatment of major bleeding.
Tranexamic acid and aminocaproic acid inhibit fibrinolysis and lead to a de facto reduced bleeding rate. Before its withdrawal, aprotinin was used in some forms of major surgery to decrease bleeding risk and the need for blood products.
Rivaroxaban drug bound to the coagulation factor Xa. The drug prevents this protein from activating the coagulation pathway by inhibiting its enzymatic activity.
Anticoagulants
Anticoagulants and anti-platelet agents (together "antithrombotics") are amongst the most commonly used medications. Anti-platelet agents include aspirin, dipyridamole, ticlopidine, clopidogrel, ticagrelor and prasugrel; the parenteral glycoprotein IIb/IIIa inhibitors are used during angioplasty. Of the anticoagulants, warfarin (and related coumarins) and heparin are the most commonly used. Warfarin affects the vitamin K-dependent clotting factors (II, VII, IX, X) and protein C and protein S, whereas heparin and related compounds increase the action of antithrombin on thrombin and factor Xa. A newer class of drugs, the direct thrombin inhibitors, is under development; some members are already in clinical use (such as lepirudin, argatroban, bivalirudin and dabigatran). Also in clinical use are other small molecular compounds that interfere directly with the enzymatic action of particular coagulation factors (the directly acting oral anticoagulants: dabigatran, rivaroxaban, apixaban, and edoxaban).
Sesamoid bone
Gist
A sesamoid bone is a small bone commonly found embedded within a muscle or tendon near joint surfaces, existing as focal areas of ossification and functioning as a pulley to alleviate stress on that particular muscle or tendon.
Summary
Sesamoid bones are small round or oval shaped nodules that are located within certain tendons. Typically there are five sesamoid bones in each hand; two at the metacarpophalangeal (MCP) joint of the thumb, one at the interphalangeal (IP) joint of the thumb, one at the MCP joint of the index finger on the radial side, and one at the MCP joint of the little finger on the ulnar side. Sesamoid bones of the thumb MCP joint located imbedded within the tendons of the FPB and the AddP. These bones act as a pulley by altering the lines of pull of the tendons in which they insert, consequently improving the efficacy of the muscles.
Details
In anatomy, a sesamoid bone is a bone embedded within a tendon or a muscle. Its name is derived from the Greek word for 'sesame seed', indicating the small size of most sesamoids. Often, these bones form in response to strain, or can be present as a normal variant. The patella is the largest sesamoid bone in the body. Sesamoids act like pulleys, providing a smooth surface for tendons to slide over, increasing the tendon's ability to transmit muscular forces.
Structure
Sesamoid bones can be found on joints throughout the human body, including:
* In the knee—the patella (within the quadriceps tendon). This is the largest sesamoid bone.
* In the hand—two sesamoid bones are commonly found in the distal portions of the first metacarpal bone (within the tendons of adductor pollicis and flexor pollicis brevis). There is also commonly a sesamoid bone in distal portions of the second metacarpal bone and fifth metacarpal bone.
* In the wrist—The pisiform of the wrist is a sesamoid bone (within the tendon of flexor carpi ulnaris). It begins to ossify in children ages 9–12.
* In the foot—the first metatarsal bone usually has two sesamoid bones at its connection to the big toe (both within the tendon of flexor hallucis brevis). One is found on the lateral side of the first metatarsal while the other is found on the medial side. In some people, only a single sesamoid is found on the first metatarsal bone.
Common variants
* One or both of the sesamoid bones under the first metatarsophalangeal joint (of the great toe) can be multipartite – in two or three parts (mostly bipartite – in two parts).
* The fabella is a small sesamoid bone found in some mammals embedded in the tendon of the lateral head of the gastrocnemius muscle behind the lateral condyle of the femur. It is a variant of normal anatomy and present in humans in 10% to 30% of individuals. The fabella can also be mutipartite or bipartite.
* The cyamella is a small sesamoid bone embedded in the tendon of the popliteus muscle. It is a variant of normal anatomy. It is rarely seen in humans, but has been described more often in other primates and certain other animals.
Clinical significance
* A common foot ailment in dancers is sesamoiditis (an inflammation of the sesamoid bones under the first metatarsophalangeal joint of the big toe). This is a form of tendinitis which results from the tendons surrounding the sesamoid becoming inflamed or irritated.
* Sesamoid bones generally have a very limited blood supply, rendering them prone to avascular necrosis (bone death from lack of blood supply), which is very difficult to treat.
Other animals
In equine anatomy, the term sesamoid bone usually refers to the two sesamoid bones found at the back of the fetlock or metacarpophalangeal and metatarsophalangeal joints in both hindlimbs and forelimbs. Strictly these should be termed the proximal sesamoid bones whereas the navicular bone should be referred to as the distal sesamoid bone. The patella is also a form of sesamoid bone in the horse.
Although many carnivores have radial sesamoid bones, the giant panda and red panda independently evolved to have an enlarged radial sesamoid bone. This evolution has caused the two species to diverge from other carnivores. The red panda likely originally evolved the "pseudo-thumb" in order to assist in arboreal locomotion. When the red panda later evolved to consume a bamboo diet, the enlarged bone underwent exaptation to assist in grasping bamboo. The giant panda, however, evolved the enlarged radial sesamoid bone around the same time as it evolved a bamboo diet. In the giant panda, the bone allows for a pincer-like motion and is used in grasping the bamboo. In these two panda species, DYNC2H1 gene and PCNT gene have been identified as possible causes for the pseudo-thumb development.
Recently, the enlarged radial sesamoid bone of cotton rats has been studied. Their enlarged radial sesamoid bone and that of the giant panda have a similar morphology and size relative to the rest of the hand. The reason for this evolutionary change is still unknown; however, it may be to assist in grasping small objects and thin branches.
Elephants have similarly enlarged sesamoid bones in both their forelimbs and hindlimbs, referred to as the prepollex and prehallux, respectively. These sesamoids function as "sixth toes", helping to distribute the animals' weight. In contrast to other sesamoids in elephants, which ossify at three to seven years of age, the ossification of the prepollex and prehallux is delayed and is known to not have yet occurred in animals in excess of 20 years of age. The prehallux is further divided into two elements; the more proximal of these is fixed, whilst the more distal is mobile. Evidence of these "predigits" has also been found in certain fossil proboscideans.
The forepaws of moles also possess a prepollex consisting of an enlarged, sickle-shaped sesamoid.
Additional Information
Sesamoid bones are a type of bone that develop in some tendons where they cross the ends of long bones. Sesamoids ossify during puberty and delayed ossification can indicate delayed onset of puberty.
Sesamoid bones in the human body include:
* Patella - in the quadriceps tendon at the knee
* Hallux sesamoids - medial/tibia and lateral/fibular in the flexor hallucis brevis tendon at the 1st metatarsophalangeal joint
* In the hand at the head of the 1st metacarpal - one in the combined tendon of the flexor pollicis brevis and abductor pollicis brevis and one in the tendon of the adductor pollicis
* Pisiform - in the flexor carpi ulnaris tendon
Function
Sesamoids protect tendons from excessive wear and act as a spacer to change the angle of tendons before the reach their attachment point. The change in angle improves muscle force generation.
Clinical relevance
Pathology in sesamoids can be congenital or a result of trauma. Common pathology seen in sesamoid bones include:
* Bipartite or multipartite patella
* Sesamoiditis
* Fracture - such as patella fracture
* Avascular necrosis
Management of the different pathologies varies depending on the diagnosis. Physiotherapy or conservative management is typically the first line of treatment for atraumatic pathology of sesamoids.
2157) William E. Moerner
Gist:
Life
W. E. Moerner was born in Pleasanton, California, but grew up in Texas. After studies at Washington University in St. Louis, Missouri and Cornell University in Ithaca, New York, in 1982 he received his doctorate from Cornell. He then worked at the IBM Almaden Research Center in San Jose, California until 1995. After three years at the University of California at San Diego, he moved to Stanford University in California. He has been a visiting professor at ETH Zurich and at Harvard University. W. E. Moerner is married and has one son.
Work
In normal microscopes the wavelength of light sets a limit to the level of detail possible. However this limitation can be circumvented by methods that make use of fluorescence, a phenomenon in which certain substances become luminous after having been exposed to light. Around 2000, Eric Betzig and William E. Moerner helped create a method in which fluorescence in individual molecules is steered by light. An image of very high resolution is achieved by combining images in which different molecules are activated. This makes it possible to track processes occurring inside living cells.
Summary
W.E. Moerner (born 1953, Pleasanton, California, U.S.) is an American chemist who won the 2014 Nobel Prize for Chemistry for his work with single-molecule spectroscopy, which paved the way for later work in single-molecule microscopy by American physicist Eric Betzig. Moerner and Betzig shared the prize with Romanian-born German chemist Stefan Hell.
Moerner received bachelor’s degrees from Washington University in St. Louis, Missouri, in 1975 in three subjects: electrical engineering, mathematics, and physics. He then received a master’s (1978) and a doctorate (1982) in physics from Cornell University in Ithaca, New York. He joined the IBM Almaden Research Center in San Jose, California, as a research staff member in 1981 and became a manager in 1988 and a project leader in 1989. In 1995 he became a professor in the chemistry and biochemistry department of the University of California, San Diego, and in 1998 he moved to Stanford University, where he was a professor of chemistry.
In 1989 Moerner and German physicist Lothar Kador were the first to observe light being absorbed by single molecules, in that case those of pentacene that were embedded in p-terphenyl crystals. That method, which they invented, came to be called single-molecule spectroscopy. In most chemical experiments, many molecules are studied, and the behaviour of a single molecule is inferred. However, single-molecule spectroscopy enables the study of what individual molecules are doing.
Moerner’s next great discovery happened in 1997 when he was working with variants of green fluorescent protein (GFP), a naturally occurring protein made by the jellyfish Aequorea victoria. Scientists often link GFP to other specific proteins, and GFP reveals their location when it fluoresces. When a single molecule of one of those variants was excited with light of a wavelength of 488 nanometres (nm), the molecule began to blink. The blinking eventually stopped despite continued doses of 488-nm light. However, when the GFP variant was excited with 405-nm light, it regained its ability to blink from 488-nm light. That control of the GFP molecule’s fluorescence meant that the proteins could act as tiny lamps within a material. That property was later exploited by Betzig, who in 2006 used other fluorescent proteins to create images of lysosomes and mitochondria at resolutions higher than the inherent limit of optical microscopy.
Details
William Esco Moerner, also known as W. E. Moerner, (born June 24, 1953) is an American physical chemist and chemical physicist with current work in the biophysics and imaging of single molecules. He is credited with achieving the first optical detection and spectroscopy of a single molecule in condensed phases, along with his postdoc, Lothar Kador. Optical study of single molecules has subsequently become a widely used single-molecule experiment in chemistry, physics and biology. In 2014, he was awarded the Nobel Prize in Chemistry.
Early life and education
Moerner was born in Pleasanton, California, in 1953 June 24 the son of Bertha Frances (Robinson) and William Alfred Moerner. He was a boy scout, with the Boy Scouts of America and became an Eagle Scout. He attended Washington University in St. Louis for undergraduate studies as an Alexander S. Langsdorf Engineering Fellow, and obtained three degrees: a B.S. in physics with Final Honors, a B.S. in electrical engineering with Final Honors, and an A.B. in mathematics summa cum laude in 1975.
He then pursued graduate study, partially supported by a National Science Foundation , at Cornell University in the group of Albert J. Sievers III. Here he received an M.S. degree and a Ph.D. degree in physics in 1978 and 1982, respectively. His doctoral thesis was on vibrational relaxation dynamics of an IR-laser-excited molecular impurity mode in alkali halide lattices. Throughout his school years, Moerner was a straight A student from 1963 to 1982, and won both the Dean's Award for Unusually Exceptional Academic Achievement as well as the Ethan A. H. Shepley Award for Outstanding Achievement when he graduated from college.
Career
Moerner worked at the IBM Almaden Research Center in San Jose, California, as a research staff member from 1981 to 1988, a manager from 1988 to 1989, and project leader from 1989 to 1995. After an appointment as visiting guest professor of physical chemistry at ETH Zurich (1993–1994), he assumed the distinguished chair in physical chemistry in the department of chemistry and biochemistry at the University of California, San Diego, from 1995 to 1998. In 1997 he was named the Robert Burns Woodward Visiting Professor at Harvard University. His research group moved to Stanford University in 1998, where he became professor of chemistry (1998), Harry S. Mosher Professor (2003), and professor, by courtesy, of applied physics (2005). Moerner was appointed department chair for chemistry from 2011 to 2014. His current areas of research and interest include: single-molecule spectroscopy and super-resolution microscopy, physical chemistry, chemical physics, biophysics, nanoparticle trapping, nanophotonics, photorefractive polymers, and spectral hole-burning. As of May 2014, Moerner was listed as a faculty advisor in 26 theses written by Stanford graduate students. As of May 16, 2014, there are 386 publications listed in Moerner's full CV.
Recent editorial and advisory boards Moerner has served on include: member of the Board of Scientific Counselors for the National Institute of Biomedical Imaging and Bioengineering (NIBIB); Advisory board member for the Institute of Atomic and Molecular Sciences, Academica Sinica, Taiwan; advisory editorial board member for Chemical Physics Letters; advisory board member for the Center for Biomedical Imaging at Stanford; and chair of Stanford University's health and safety committee.
Awards and honors
Moerner is the recipient the National Winner of the Outstanding Young Professional Award for 1984, from the electrical engineering honorary society, Eta Kappa Nu, April 22, 1985; IBM Outstanding Technical Achievement Award for Photon-Gated Spectral Hole-Burning, July 11, 1988; IBM Outstanding Technical Achievement Award for Single-Molecule Detection and Spectroscopy, November 22, 1992; Earle K. Plyler Prize for Molecular Spectroscopy, American Physical Society, 2001; Wolf Prize in Chemistry, 2008; Irving Langmuir Award in Chemical Physics, American Physical Society, 2009; Pittsburgh Spectroscopy Award, 2014; Peter Debye Award in Physical Chemistry, American Chemical Society, 2013; the Engineering Alumni Achievement Award, Washington University, 2013; and the Nobel Prize in Chemistry, 2014. Moerner also holds more than a dozen patents.
His honorary memberships include Senior Member, IEEE, June 17, 1988, and Member, National Academy of Sciences, 2007. He is also a Fellow of the Optical Society of America, May 28, 1992; the American Physical Society, November 16, 1992; the American Academy of Arts and Sciences, 2001; and the American Association for the Advancement of Science, 2004.
Personal life
Moerner was born on June 24, 1953, at Parks Air Force Base in Pleasanton, California. From birth, his family called him by his initials W. E. as a way to distinguish him from his father and grandfather who are also named William. He grew up in Texas where he attended Thomas Jefferson High School in San Antonio. He participated in many activities during high school: Band, Speech and Debate, Math and Science Contest Team, Bi-Phy-Chem, Masque and Gavel, National Honor Society, Boy Scouts, Amateur Radio Club, Russian Club, Forum Social Club, Toastmasters, "On the Spot" Team and Editor of Each has Spoken. Moerner and his wife, Sharon, have one son, Daniel.
Additional Information
William Esco Moerner (born June 24, 1953) is an American physical chemist and chemical physicist.
He is known for his first optical detection and spectroscopy of a single molecule in condensed phases. Optical study of single molecules has subsequently become a widely used single-molecule experiment in chemistry, physics and biology.
In 2014, he was awarded the Nobel Prize in Chemistry.
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