Posts by Jai Ganesh

Jai Ganesh · Dark Discussions at Cafe Infinity

2450) Linus Pauling

Gist:

Life

Linus Pauling was born in Portland, Oregon, in the United States. His family came from a line of Prussian farmers, and Pauling's father worked as a pharmaceuticals salesman, among other things. After first studying at Oregon State University in Corvallis, Oregon, Pauling earned his PhD from the California Institute of Technology in Pasadena, with which he maintained ties for the rest of his career. In the 1950s, Pauling's involvement in the anti-nuclear movement led to his being labeled a suspected communist, which resulted in his passport being revoked at times. Linus and Ava Helen Pauling had four children together.

Work

The development of quantum mechanics during the 1920s had a great impact not only on the field of physics, but also on chemistry. During the 1930s Linus Pauling was among the pioneers who used quantum mechanics to understand and describe chemical bonding–that is, the way atoms join together to form molecules. Pauling worked in a broad range of areas within chemistry. For example, he worked on the structures of biologically important chemical compounds. In 1951 he published the structure of the alpha helix, which is an important basic component of many proteins.

Summary

Linus Carl Pauling (February 28, 1901 – August 19, 1994) was an American chemist and peace activist. He published more than 1,200 papers and books, of which about 850 dealt with scientific topics. New Scientist called him one of the 20 greatest scientists of all time. For his scientific work, Pauling was awarded the Nobel Prize in Chemistry in 1954. For his peace activism, he was awarded the Nobel Peace Prize in 1962. He is one of five people to have won more than one Nobel Prize. Of these, he is the only person to have been awarded two unshared Nobel Prizes, and one of two people to be awarded Nobel Prizes in different fields, the other being Marie Skłodowska-Curie.

Pauling was one of the founders of the fields of quantum chemistry and molecular biology. His contributions to the theory of the chemical bond include the concept of orbital hybridisation and the first accurate scale of electronegativities of the elements. Pauling also worked on the structures of biological molecules, and showed the importance of the alpha helix and beta sheet in protein secondary structure. Pauling's approach combined methods and results from X-ray crystallography, molecular model building, and quantum chemistry. His discoveries inspired the work of James Watson, Francis Crick, Rosalind Franklin, and Maurice Wilkins on the structure of DNA, which in turn made it possible for geneticists to crack the DNA code of all organisms.

In his later years, he promoted nuclear disarmament, as well as orthomolecular medicine, megavitamin therapy, and dietary supplements, especially ascorbic acid (commonly known as Vitamin C). None of his ideas concerning the medical usefulness of large doses of vitamins have gained much acceptance in the mainstream scientific community. He was married to the American human rights activist Ava Helen Pauling.

Details

Linus Pauling (born February 28, 1901, Portland, Oregon, U.S.—died August 19, 1994, Big Sur, California) was an American theoretical physical chemist who became the only person to have won two unshared Nobel Prizes. His first prize (1954) was awarded for research into the nature of the chemical bond and its use in elucidating molecular structure; the second (1962) recognized his efforts to ban the testing of nuclear weapons.

Early life and education

Pauling was the first of three children and the only son of Herman Pauling, a pharmacist, and Lucy Isabelle (Darling) Pauling, a pharmacist’s daughter. After his early education in Condon and Portland, Oregon, he attended Oregon Agricultural College (now Oregon State University), where he met Ava Helen Miller, who would later become his wife, and where he received his Bachelor of Science degree in chemical engineering summa cum laude in 1922. He then attended the California Institute of Technology (Caltech), where Roscoe G. Dickinson showed him how to determine the structures of crystals using X rays. He received his Ph.D. in 1925 for a dissertation derived from his crystal-structure papers. Following a brief period as a National Research Fellow, he received a Guggenheim Fellowship to study quantum mechanics in Europe. He spent most of the 18 months at Arnold Sommerfeld’s Institute for Theoretical Physics in Munich, Germany.

Elucidation of molecular structures

After completing postdoctoral studies, Pauling returned to Caltech in 1927. There he began a long career of teaching and research. Analyzing chemical structure became the central theme of his scientific work. By using the technique of X-ray diffraction, he determined the three-dimensional arrangement of atoms in several important silicate and sulfide minerals. In 1930, during a trip to Germany, Pauling learned about electron diffraction, and upon his return to California he used this technique of scattering electrons from the nuclei of molecules to determine the structures of some important substances. This structural knowledge assisted him in developing an electronegativity scale in which he assigned a number representing a particular atom’s power of attracting electrons in a covalent bond.

To complement the experimental tool that X-ray analysis provided for exploring molecular structure, Pauling turned to quantum mechanics as a theoretical tool. For example, he used quantum mechanics to determine the equivalent strength in each of the four bonds surrounding the carbon atom. He developed a valence bond theory in which he proposed that a molecule could be described by an intermediate structure that was a resonance combination (or hybrid) of other structures. His book The Nature of the Chemical Bond, and the Structure of Molecules and Crystals (1939) provided a unified summary of his vision of structural chemistry.

The arrival of the geneticist Thomas Hunt Morgan at Caltech in the late 1920s stimulated Pauling’s interest in biological molecules, and by the mid-1930s he was performing successful magnetic studies on the protein hemoglobin. He developed further interests in protein and, together with biochemist Alfred Mirsky, Pauling published a paper in 1936 on general protein structure. In this work the authors explained that protein molecules naturally coiled into specific configurations but became “denatured” (uncoiled) and assumed some random form once certain weak bonds were broken.

On one of his trips to visit Mirsky in New York, Pauling met Karl Landsteiner, the discoverer of blood types, who became his guide into the field of immunochemistry. Pauling was fascinated by the specificity of antibody-antigen reactions, and he later developed a theory that accounted for this specificity through a unique folding of the antibody’s polypeptide chain. World War II interrupted this theoretical work, and Pauling’s focus shifted to more practical problems, including the preparation of an artificial substitute for blood serum useful to wounded soldiers and an oxygen detector useful in submarines and airplanes. J. Robert Oppenheimer asked Pauling to head the chemistry section of the Manhattan Project, but his suffering from glomerulonephritis (inflammation of the glomerular region of the kidney) prevented him from accepting this offer. For his outstanding services during the war, Pauling was later awarded the Presidential Medal for Merit.

While collaborating on a report about postwar American science, Pauling became interested in the study of sickle-cell anemia. He perceived that the sickling of cells noted in this disease might be caused by a genetic mutation in the globin portion of the blood cell’s hemoglobin. In 1949 he and his coworkers published a paper identifying the particular defect in hemoglobin’s structure that was responsible for sickle-cell anemia, which thereby made this disorder the first “molecular disease” to be discovered. At that time, Pauling’s article on the periodic law appeared in the 14th edition of Encyclopædia Britannica.

While serving as a visiting professor at the University of Oxford in 1948, Pauling returned to a problem that had intrigued him in the late 1930s—the three-dimensional structure of proteins. By folding a paper on which he had drawn a chain of linked amino acids, he discovered a cylindrical coil-like configuration, later called the alpha helix. The most significant aspect of Pauling’s structure was its determination of the number of amino acids per turn of the helix. During this same period he became interested in deoxyribonucleic acid (DNA), and early in 1953 he and protein crystallographer Robert Corey published their version of DNA’s structure, three strands twisted around each other in ropelike fashion. Shortly thereafter James Watson and Francis Crick published DNA’s correct structure, a double helix. Pauling’s efforts to modify his postulated structure had been hampered by poor X-ray photographs of DNA and by his lack of understanding of this molecule’s wet and dry forms. In 1952 he failed to visit Rosalind Franklin, working in Maurice Wilkins’s laboratory at King’s College, London, and consequently did not see her X-ray pictures of DNA. Frankin’s pictures proved to be the linchpin in allowing Watson and Crick to elucidate the actual structure. Nevertheless, Pauling was awarded the 1954 Nobel Prize for Chemistry “for his research into the nature of the chemical bond and its application to the elucidation of the structure of complex substances.”

Humanitarian activities of Linus Pauling

During the 1950s Pauling and his wife became well known to the public through their crusade to stop the atmospheric testing of nuclear weapons. In 1958 they presented an appeal for a test ban to the United Nations in the form of a document signed by 9,235 scientists from 44 countries. Pauling’s sentiments were also promulgated through his book No More War! (1958), a passionate analysis of the implications of nuclear war for humanity. In 1960 he was called upon to defend his actions regarding a test ban before a congressional subcommittee. By refusing to reveal the names of those who had helped him collect signatures, he risked going to jail—a stand initially condemned but later widely admired. His work on behalf of world peace was recognized with the 1962 Nobel Prize for Peace awarded on October 10, 1963, the date that the Nuclear Test Ban Treaty went into effect.

Pauling’s Peace Prize generated such antagonism from Caltech administrators that he left the institute in 1963. He became a staff member at the Center for the Study of Democratic Institutions in Santa Barbara, California, where his humanitarian work was encouraged. Although he was able to develop a new model of the atomic nucleus while working at the Center, his desire to perform more experimental research led him to a research professorship at the University of California in San Diego in 1967. There he published a paper on orthomolecular psychiatry that explained how mental health could be achieved by manipulating substances normally present in the body. Two years later he accepted a post at Stanford University, where he worked until 1972.

Later years

While at San Diego and Stanford, Pauling’s scientific interests centred on a particular molecule—ascorbic acid (vitamin C). He examined the published reports about this vitamin and concluded that, when taken in large enough quantities (megadoses), it would help the body fight off colds and other diseases. The outcome of his research was the book Vitamin C and the Common Cold (1970), which became a best-seller. Pauling’s interest in vitamin C in particular and orthomolecular medicine in general led, in 1973, to his founding an institute that eventually bore his name—the Linus Pauling Institute of Science and Medicine. During his tenure at this institute, he became embroiled in controversies about the relative benefits and risks of ingesting megadoses of various vitamins. The controversy intensified when he advocated vitamin C’s usefulness in the treatment of cancer. Pauling and his collaborator, the Scottish physician Ewan Cameron, published their views in Cancer and Vitamin C (1979). Their ideas were subjected to experimental animal studies funded by the institute. While these studies supported their ideas, investigations at the Mayo Clinic involving human cancer patients did not corroborate Pauling’s results.

Although he continued to receive recognition for his earlier accomplishments, Pauling’s later work provoked considerable skepticism and controversy. His cluster model of the atomic nucleus was rejected by physicists, his interpretation of the newly discovered quasicrystals received little support, and his ideas on vitamin C were rejected by the medical establishment. In an effort to raise money to support his increasingly troubled institute, Pauling published How to Live Longer and Feel Better (1986), but the book failed to become the success that he and his associates had anticipated.

Both Pauling and his wife developed cancer. Ava Helen Pauling died of stomach cancer in 1981. Ten years later Pauling discovered that he had prostate cancer. Although he underwent surgery and other treatments, the cancer eventually spread to his liver. He died at his ranch on the Big Sur coast of California.

Jai Ganesh · This is Cool

2513) Neurotransmitters

Gist

Neurotransmitters are endogenous chemical messengers that transmit signals across a synapse from one neuron to another target cell (neuron, muscle, or gland). They are vital for brain function, influencing mood, sleep, memory, and motor control. Over 50 types exist, acting as either excitatory (triggering a response) or inhibitory (inhibiting a response).

Neurotransmitters are often referred to as the body's chemical messengers. They are the molecules used by the nervous system to transmit messages between neurons, or from neurons to muscles.

Neurotransmitters are endogenous chemical messengers that transmit signals across a synapse between neurons, muscles, or gland cells, essential for regulating body functions, emotions, and thoughts. They are classified into amino acids, peptides, monoamines, purines, and gasotransmitters, with over 50 types known. Their action is either excitatory (promoting a signal) or inhibitory (stopping a signal).

Summary

A neurotransmitter is a signaling molecule secreted by a neuron to affect another cell across a synapse. The cell receiving the signal, or target cell, may be another neuron, but could also be a gland or muscle cell.

Neurotransmitters are released from synaptic vesicles into the synaptic cleft where they are able to interact with neurotransmitter receptors on the target cell. Some neurotransmitters are also stored in large dense core vesicles. The neurotransmitter's effect on the target cell is determined by the receptor it binds to. Many neurotransmitters are synthesized from simple and plentiful precursors such as amino acids, which are readily available and often require a small number of biosynthetic steps for conversion.

Neurotransmitters are essential to the function of complex neural systems. The exact number of unique neurotransmitters in humans is unknown, but more than 100 have been identified. Common neurotransmitters include glutamate, GABA, acetylcholine, glycine, dopamine and norepinephrine.

(GABA: gamma-aminobutyric acid).

Details

Neurotransmitters are your body’s chemical messengers. They carry messages from one nerve cell across a space to the next nerve, muscle or gland cell. These messages help you move your limbs, feel sensations, keep your heart beating, and take in and respond to all information your body receives from other internal parts of your body and your environment.

What are neurotransmitters?

Neurotransmitters are chemical messengers that your body can’t function without. Their job is to carry chemical signals (“messages”) from one neuron (nerve cell) to the next target cell. The next target cell can be another nerve cell, a muscle cell or a gland.

Your body has a vast network of nerves (your nervous system) that send and receive electrical signals from nerve cells and their target cells all over your body. Your nervous system controls everything from your mind to your muscles, as well as organ functions. In other words, nerves are involved in everything you do, think and feel. Your nerve cells send and receive information from all body sources. This constant feedback is essential to your body’s optimal function.

What body functions do nerves and neurotransmitters help control?

Your nervous system controls such functions as your:

* Heartbeat and blood pressure.
* Breathing.
* Muscle movements.
* Thoughts, memory, learning and feelings.
* Sleep, healing and aging.
* Stress response.
* Hormone regulation.
* Digestion, sense of hunger and thirst.
* Senses (response to what you see, hear, feel, touch and taste).

How do neurotransmitters work?

You have billions of nerve cells in your body. Nerve cells are generally made up of three parts:

* A cell body. The cell body is vital to producing neurotransmitters and maintaining the function of the nerve cell.
* An axon. The axon carries the electrical signals along the nerve cell to the axon terminal.
* An axon terminal. This is where the electrical message is changed to a chemical signal using neurotransmitters to communicate with the next group of nerve cells, muscle cells or organs.

Neurotransmitters are located in a part of the neuron called the axon terminal. They’re stored within thin-walled sacs called synaptic vesicles. Each vesicle can contain thousands of neurotransmitter molecules.

As a message or signal travels along a nerve cell, the electrical charge of the signal causes the vesicles of neurotransmitters to fuse with the nerve cell membrane at the very edge of the cell. The neurotransmitters, which now carry the message, are then released from the axon terminal into a fluid-filled space that’s between one nerve cell and the next target cell (another nerve cell, muscle cell or gland).

In this space, called the synaptic junction, the neurotransmitters carry the message across less than 40 nanometers (nm) wide (by comparison, the width of a human hair is about 75,000 nm). Each type of neurotransmitter lands on and binds to a specific receptor on the target cell (like a key that can only fit and work in its partner lock). After binding, the neurotransmitter then triggers a change or action in the target cell, like an electrical signal in another nerve cell, a muscle contraction or the release of hormones from a cell in a gland.

What action or change do neurotransmitters transmit to the target cell?

Neurotransmitters transmit one of three possible actions in their messages, depending on the specific neurotransmitter.

* Excitatory. Excitatory neurotransmitters “excite” the neuron and cause it to “fire off the message,” meaning, the message continues to be passed along to the next cell. Examples of excitatory neurotransmitters include glutamate, epinephrine and norepinephrine.
* Inhibitory. Inhibitory neurotransmitters block or prevent the chemical message from being passed along any farther. Gamma-aminobutyric acid (GABA), glycine and serotonin are examples of inhibitory neurotransmitters.
* Modulatory. Modulatory neurotransmitters influence the effects of other chemical messengers. They “tweak” or adjust how cells communicate at the synapse. They also affect a larger number of neurons at the same time.

What happens to neurotransmitters after they deliver their message?

After neurotransmitters deliver their message, the molecules must be cleared from the synaptic cleft (the space between the nerve cell and the next target cell). They do this in one of three ways.

Neurotransmitters:

* Fade away (a process called diffusion).
* Are reabsorbed and reused by the nerve cell that released it (a process called reuptake).
* Are broken down by enzymes within the synapse so it can’t be recognized or bind to the receptor cell (a process called degradation).

How many different types of neurotransmitters are there?

Scientists know of at least 100 neurotransmitters and suspect there are many others that have yet to be discovered. They can be grouped into types based on their chemical nature. Some of the better-known categories and neurotransmitter examples and their functions include the following:

Amino acids neurotransmitters

These neurotransmitters are involved in most functions of your nervous system.

* Glutamate. This is the most common excitatory neurotransmitter of your nervous system. It’s the most abundant neurotransmitter in your brain. It plays a key role in cognitive functions like thinking, learning and memory. Imbalances in glutamate levels are associated with Alzheimer’s disease, dementia, Parkinson’s disease and seizures.
* Gamma-aminobutryic acid (GABA). GABA is the most common inhibitory neurotransmitter of your nervous system, particularly in your brain. It regulates brain activity to prevent problems in the areas of anxiety, irritability, concentration, sleep, seizures and depression.
* Glycine. Glycine is the most common inhibitory neurotransmitter in your spinal cord. Glycine is involved in controlling hearing processing, pain transmission and metabolism.

Monoamines neurotransmitters

These neurotransmitters play a lot of different roles in your nervous system and especially in your brain. Monoamines neurotransmitters regulate consciousness, cognition, attention and emotion. Many disorders of your nervous system involve abnormalities of monoamine neurotransmitters, and many drugs that people commonly take affect these neurotransmitters.

* Serotonin. Serotonin is an inhibitory neurotransmitter. Serotonin helps regulate mood, sleep patterns, sexuality, anxiety, appetite and pain. Diseases associated with serotonin imbalance include seasonal affective disorder, anxiety, depression, fibromyalgia and chronic pain. Medications that regulate serotonin and treat these disorders include selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs).
* Histamine. Histamine regulates body functions including wakefulness, feeding behavior and motivation. Histamine plays a role in asthma, bronchospasm, mucosal edema and multiple sclerosis.
* Dopamine. Dopamine plays a role in your body’s reward system, which includes feeling pleasure, achieving heightened arousal and learning. Dopamine also helps with focus, concentration, memory, sleep, mood and motivation. Diseases associated with dysfunctions of the dopamine system include Parkinson’s disease, schizophrenia, bipolar disease, restless legs syndrome and attention deficit hyperactivity disorder (ADHD). Many highly addictive drugs (cocaine, methamphetamines, amphetamines) act directly on the dopamine system.
* Epinephrine. Epinephrine (also called adrenaline) and norepinephrine (see below) are responsible for your body’s so-called “fight-or-flight response” to fear and stress. These neurotransmitters stimulate your body’s response by increasing your heart rate, breathing, blood pressure, blood sugar and blood flow to your muscles, as well as heighten attention and focus to allow you to act or react to different stressors. Too much epinephrine can lead to high blood pressure, diabetes, heart disease and other health problems. As a drug, epinephrine is used to treat anaphylaxis, asthma attacks, cardiac arrest and severe infections.
* Norepinephrine. Norepinephrine (also called noradrenaline) increases blood pressure and heart rate. It’s most widely known for its effects on alertness, arousal, decision-making, attention and focus. Many medications (stimulants and depression medications) aim to increase norepinephrine levels to improve focus or concentration to treat ADHD or to modulate norepinephrine to improve depression symptoms.

Peptide neurotransmitters

Peptides are polymers or chains of amino acids.

* Endorphins. Endorphins are your body’s natural pain reliever. They play a role in our perception of pain. Release of endorphins reduces pain, as well as causes “feel good” feelings. Low levels of endorphins may play a role in fibromyalgia and some types of headaches.

Acetylcholine

This excitatory neurotransmitter does a number of functions in your central nervous system (CNS [brain and spinal cord]) and in your peripheral nervous system (nerves that branch from the CNS). Acetylcholine is released by most neurons in your autonomic nervous system regulating heart rate, blood pressure and gut motility. Acetylcholine plays a role in muscle contractions, memory, motivation, sexual desire, sleep and learning. Imbalances in acetylcholine levels are linked with health issues, including Alzheimer’s disease, seizures and muscle spasms.

Why would a neurotransmitter not work as it should?

Several things can go haywire and lead to neurotransmitters not working as they should. In general, some of these problems include:

* Too much or not enough of one or more neurotransmitters are produced or released.
* The receptor on the receiver cell (the nerve, muscle or gland) isn’t working properly. The otherwise normal functioning neurotransmitter can’t effectively signal the next cell.
* The cell receptors aren’t taking up enough neurotransmitter due to inflammation and damage of the synaptic cleft.
* Neurotransmitters are reabsorbed too quickly.
* Enzymes limit the number of neurotransmitters from reaching their target cell.

Problems with other parts of nerves, existing diseases or medications you may be taking can affect neurotransmitters. Also, when neurotransmitters don’t function as they should, disease can happen. For example:

* Not enough acetylcholine can lead to the loss of memory that’s seen in Alzheimer’s disease.
* Too much serotonin is possibly associated with autism spectrum disorders.
* An increase in activity of glutamate or reduced activity of GABA can result in sudden, high-frequency firing of local neurons in your brain, which can cause seizures.
* Too much norepinephrine and dopamine activity and abnormal glutamate transmission contribute to mania.

How do medications affect the action of neurotransmitters?

Scientists recognized the value and the role of neurotransmitters in your nervous system and the importance of developing medications that could influence these chemical messengers to treat many health conditions. Many medications, especially those that treat diseases of your brain, work in many ways to affect neurotransmitters.

Medications can block the enzyme that breaks down a neurotransmitter so that more of it reaches nerve receptors.

Example: Donepezil, galantamine and rivastigmine block the enzyme acetylcholinesterase, which breaks down the neurotransmitter acetylcholine. These medications are used to stabilize and improve memory and cognitive function in people with Alzheimer’s disease, as well as other neurodegenerative disorders.

Medications can block the neurotransmitter from being received at its receptor site.

Example: Selective serotonin reuptake inhibitors are a type of drug class that blocks serotonin from being received and absorbed by a nerve cell. These drugs may be helpful in treating depression, anxiety and other mental health conditions.

Medications can block the release of a neurotransmitter from a nerve cell.

Example: Lithium works as a treatment for mania partially by blocking norepinephrine release and is used in the treatment of bipolar disorder.

Additional Information

Neurotransmitters are chemical messengers in the body. Their function is to transmit signals from nerve cells to target cells. These signals help regulate bodily functions ranging from heart rate to appetite.

Neurotransmitters are part of the nervous system. They play a crucial role in human development and many bodily functions.

What is a neurotransmitter?

The nervous system controls the body’s organs and plays a role in nearly all bodily functions. Nerve cells, also known as neurons, and their neurotransmitters play important roles in this system.

Nerve cells fire nerve impulses. They do this by releasing neurotransmitters, also known as the body’s chemical messengers. These chemicals carry signals to other cells.

Neurotransmitters relay their messages by traveling between cells and attaching to specific receptors on target cells.

Each neurotransmitter attaches to a different receptor. For example, dopamine molecules attach to dopamine receptors. When they attach, it triggers an action in the target cells.

After neurotransmitters deliver their messages, the body breaks them down or recycles them.

What do neurotransmitters do?

The brain needs neurotransmitters to regulate many necessary functions, including:

* heart rate
* breathing
* sleep cycles
* digestion
* mood
* concentration
* appetite
* muscle movement

Neurotransmitters also play a role in early human development.

Types of neurotransmitters

Experts have identified over 100 neurotransmitters to date and are still discovering more.

Neurotransmitters have different types of actions:

* Excitatory neurotransmitters encourage a target cell to take action.
* Inhibitory neurotransmitters decrease the chances of the target cell taking action. In some cases, these neurotransmitters have a relaxation-like effect.
* Modulatory neurotransmitters can send messages to many neurons at the same time. They also communicate with other neurotransmitters.

Some neurotransmitters can carry out several functions depending on the type of receptor they connect to.

Jai Ganesh · Jokes

Q: Why did the skittles go to school?
A: Because they wanted to be smarties!
* * *
Q: How do you make a fruit punch?
A: Give it boxing lessons.
* * *
Q: Did you hear about the angry pancake?
A: He just flipped.
* * *
Q: Why did the pecans run across the busy road?
A: Because they were nuts!
* * *
Q: What is pink, goes in hard and dry and comes out soft and wet?
A: Bubble Gum.
* * *

Jai Ganesh · Dark Discussions at Cafe Infinity

Come Quotes - XXII

1. Nothing else in the world... not all the armies... is so powerful as an idea whose time has come. - Victor Hugo

2. Non-violence, which is the quality of the heart, cannot come by an appeal to the brain. - Mahatma Gandhi

3. When we are born we cry that we are come to this great stage of fools. - William Shakespeare

4. Walk while ye have the light, lest darkness come upon you. - John Ruskin

5. The goal towards which the pleasure principle impels us - of becoming happy - is not attainable: yet we may not - nay, cannot - give up the efforts to come nearer to realization of it by some means or other. - Sigmund Freud

6. When we understand string theory, we will know how the universe began. It won't have much effect on how we live, but it is important to understand where we come from and what we can expect to find as we explore. - Stephen Hawking

7. Let us more and more insist on raising funds of love, of kindness, of understanding, of peace. Money will come if we seek first the Kingdom of God - the rest will be given. - Mother Teresa

8. I balanced all, brought all to mind, the years to come seemed waste of breath, a waste of breath the years behind, in balance with this life, this death. - William Butler Yeats.

Jai Ganesh · This is Cool

River Amazon

Gist

The Amazon River in South America is the world's largest river by discharge volume, carrying more water than the next eight largest rivers combined. It is generally considered the second longest (approx. 6,400 km/4,000 miles) after the Nile, though some studies claim it is longer. Originating in the Andes, it traverses Peru, Colombia, and Brazil, emptying into the Atlantic Ocean.

The Amazon River in South America is the largest river by discharge volume of water in the world, and the longest or second-longest river system in the world, a title which is disputed with the Nile.

Summary

The Amazon River in South America is the largest river by discharge volume of water in the world, and the longest or second-longest river system in the world, a title which is disputed with the Nile.

The headwaters of the Apurímac River on Nevado Mismi had been considered, for nearly a century, the Amazon basin's most distant source until a 2014 study found it to be the headwaters of the Mantaro River on the Cordillera Rumi Cruz in Peru. The Mantaro and Apurímac rivers join, and with other tributaries form the Ucayali River, which in turn meets the Marañón River upstream of Iquitos, Peru, forming what countries other than Brazil consider to be the main stem of the Amazon. Brazilians call this section the Solimões River above its confluence with the Rio Negro forming what Brazilians call the Amazon at the Meeting of Waters (Portuguese: Encontro das Águas) at Manaus, the largest city on the river.

The Amazon River has an average discharge of about 215,000–230,000 cubic meters per second (7,600,000–8,100,000 cu ft/s)—approximately 6,591–7,570 cubic kilometers (1,581–1,816 cu mi) per year, greater than the next seven largest independent rivers combined. Two of the top ten rivers by discharge are tributaries of the Amazon river. The Amazon represents 20% of the global riverine discharge into oceans. The Amazon basin is the largest drainage basin in the world, with an area of approximately 7,000,000 square kilometers (2,700,000 sq mi). The portion of the river's drainage basin in Brazil alone is larger than any other river's basin. The Amazon enters Brazil with only one-fifth of the flow it finally discharges into the Atlantic Ocean, yet already has a greater flow at this point than the discharge of any other river in the world. It has a recognized length of 6,400 kilometers (4,000 mi), but according to some reports, its length varies from 6,575–7,062 kilometers (4,086–4,388 mi).

Details

Amazon River is the greatest river of South America and the largest drainage system in the world in terms of the volume of its flow and the area of its basin. The total length of the river—as measured from the headwaters of the Ucayali-Apurímac river system in southern Peru—is at least 4,000 miles (6,400 km), which makes it slightly shorter than the Nile River but still the equivalent of the distance from New York City to Rome. Its westernmost source is high in the Andes Mountains, within 100 miles (160 km) of the Pacific Ocean, and its mouth is in the Atlantic Ocean, on the northeastern coast of Brazil. However, both the length of the Amazon and its ultimate source have been subjects of debate since the mid-20th century, and there are those who claim that the Amazon is actually longer than the Nile. (See below The length of the Amazon.)

The vast Amazon basin (Amazonia), the largest lowland in Latin America, has an area of about 2.7 million square miles (7 million square km) and is nearly twice as large as that of the Congo River, the Earth’s other great equatorial drainage system. Stretching some 1,725 miles (2,780 km) from north to south at its widest point, the basin includes the greater part of Brazil and Peru, significant parts of Colombia, Ecuador, and Bolivia, and a small area of Venezuela; roughly two-thirds of the Amazon’s main stream and by far the largest portion of its basin are within Brazil. The Tocantins-Araguaia catchment area in Pará state covers another 300,000 square miles (777,000 square km). Although considered a part of Amazonia by the Brazilian government and in popular usage, it is technically a separate system. It is estimated that about one-fifth of all the water that runs off Earth’s surface is carried by the Amazon. The flood-stage discharge at the river’s mouth is four times that of the Congo and more than 10 times the amount carried by the Mississippi River. This immense volume of fresh water dilutes the ocean’s saltiness for more than 100 miles (160 km) from shore.

The extensive lowland areas bordering the main river and its tributaries, called várzeas (“floodplains”), are subject to annual flooding, with consequent soil enrichment; however, most of the vast basin consists of upland, well above the inundations and known as terra firme. More than two-thirds of the basin is covered by an immense rainforest, which grades into dry forest and savanna on the higher northern and southern margins and into montane forest in the Andes to the west. The Amazon Rainforest, which represents about half of the Earth’s remaining rainforest, also constitutes its single largest reserve of biological resources.

Since the later decades of the 20th century, the Amazon basin has attracted international attention because human activities have increasingly threatened the equilibrium of the forest’s highly complex ecology. Deforestation has accelerated, especially south of the Amazon River and on the piedmont outwash of the Andes, as new highways and air transport facilities have opened the basin to a tidal wave of settlers, corporations, and researchers. Significant mineral discoveries have brought further influxes of population. The ecological consequences of such developments, potentially reaching well beyond the basin and even gaining worldwide importance, have attracted considerable scientific attention.

The first European to explore the Amazon, in 1541, was the Spanish soldier Francisco de Orellana, who gave the river its name after reporting pitched battles with tribes of female warriors, whom he likened to the Amazons of Greek mythology. Although the name Amazon is conventionally employed for the entire river, in Peruvian and Brazilian nomenclature it properly is applied only to sections of it. In Peru the upper main stream (fed by numerous tributaries flowing from sources in the Andes) down to the confluence with the Ucayali River is called Marañón, and from there to the Brazilian border it is called Amazonas. In Brazil the name of the river that flows from Peru to its confluence with the Negro River is Solimões; from the Negro out to the Atlantic the river is called Amazonas.

Additional Information

Occupying much of Brazil and Peru, and also parts of Guyana, Colombia, Ecuador, Bolivia, Suriname, French Guiana, and Venezuela, the Amazon River Basin is the world’s largest drainage system. The Amazon Basin supports the world’s largest rainforest, which accounts for more than half the total volume of rainforests in the world.

The Amazon River is the second longest river in the world, flowing through South America. It is also the largest river by volume, carrying more water than all of the other rivers in the world combined. The Amazon River basin is home to the largest rainforest in the world, which is home to an incredible diversity of plant and animal life. The Amazon River is also a vital resource for the people of South America, providing food, water, and transportation. However, the Amazon River is also facing a number of threats, including deforestation, pollution, and climate change.

Amazon River – Discharge

The Amazon River is the largest river in the world by volume, with a discharge of approximately 209,000 cubic meters per second. This means that the Amazon River carries more water than all of the other rivers in the world combined. The Amazon River’s discharge is so large that it can be seen from space.

The Amazon River’s discharge is driven by the rainfall in the Amazon rainforest. The Amazon rainforest is one of the wettest places on Earth, with an average annual rainfall of over 2,000 millimeters (mm). This rainfall creates a large amount of runoff, which flows into the Amazon River.

The Amazon River’s discharge also varies throughout the year. During the wet season, from January to May, the Amazon River’s discharge can reach up to 300,000 m³/s. During the dry season, from June to December, the Amazon River’s discharge can drop to as low as 100,000 cubic meters per second.

The Amazon River’s discharge has a significant impact on the environment. The Amazon River’s discharge provides water for the Amazon rainforest, which is home to a vast array of plant and animal life. The Amazon River’s discharge also helps to regulate the climate in the Amazon rainforest.

The Amazon River’s discharge is also important to humans. The Amazon River is a major source of water for drinking, irrigation, and transportation. The Amazon River is also a major source of food, with fish being a staple of the diet of many people who live in the Amazon rainforest.

Here are some examples of the Amazon River’s discharge:

* The Amazon River’s discharge is so large that it can be seen from space.
* The Amazon River’s discharge is greater than the combined discharge of all of the other rivers in the world.
* The Amazon River’s discharge varies throughout the year, with the highest discharge occurring during the wet season and the lowest discharge occurring during the dry season.
* The Amazon River’s discharge has a significant impact on the environment, providing water for the Amazon rainforest, regulating the climate, and supporting a vast array of plant and animal life.
* The Amazon River’s discharge is also important to humans, providing water for drinking, irrigation, transportation, and food.

Amazon River Basin

The Amazon River Basin is the largest drainage basin in the world, covering an area of approximately 7 million square kilometers (2.7 million square miles). It is located in South America and includes parts of Brazil, Peru, Bolivia, Ecuador, Colombia, and Venezuela. The Amazon River is the main waterway of the basin and is the second longest river in the world, after the Nile River.

Geography

The Amazon River Basin is a vast, lowland region that is covered in dense rainforest. The basin is bordered by the Andes Mountains to the west, the Guiana Highlands to the north, and the Brazilian Highlands to the south. The Amazon River flows from the Andes Mountains in Peru and empties into the Atlantic Ocean near the city of Belém, Brazil.

Climate

The Amazon River Basin has a tropical climate, with high temperatures and abundant rainfall throughout the year. The average temperature in the basin is around 25 degrees Celsius (77 degrees Fahrenheit). The rainy season lasts from December to May, and the dry season lasts from June to November.

Biodiversity

The Amazon River Basin is one of the most biodiverse regions on Earth. It is home to an estimated 10% of the world’s known species, including many endangered species. Some of the most iconic animals of the Amazon River Basin include the jaguar, the giant anteater, the sloth, and the piranha.

Human Activity

The Amazon River Basin is home to a large population of people, including indigenous peoples, settlers, and migrants. The main economic activities in the basin are agriculture, logging, mining, and fishing. However, these activities have also led to environmental problems, such as deforestation, pollution, and climate change.

Conservation

The Amazon River Basin is a vital ecosystem that provides a number of important services, such as regulating the climate, providing food and water, and supporting biodiversity. However, the basin is facing a number of threats, including deforestation, pollution, and climate change. Conservation efforts are underway to protect the Amazon River Basin and its biodiversity.

Examples of Conservation Efforts

* The Brazilian government has created a number of protected areas in the Amazon River Basin, including national parks, wildlife refuges, and sustainable development reserves.
* The Amazon Conservation Association (ACA) is a non-profit organization that works to protect the Amazon River Basin and its biodiversity. The ACA supports sustainable development projects, promotes education and research, and advocates for policies that protect the Amazon.
* The World Wildlife Fund (WWF) is another non-profit organization that works to protect the Amazon River Basin. The WWF supports conservation projects, raises awareness about the importance of the Amazon, and advocates for policies that protect the environment.

These are just a few examples of the many conservation efforts that are underway to protect the Amazon River Basin. By working together, we can help to ensure that this vital ecosystem is preserved for future generations.

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Jai Ganesh · Science HQ

Cataract

Gist

A cataract is the gradual clouding of the eye's natural lens, usually caused by aging, which results in hazy vision, light sensitivity, and faded colors. Primarily affecting adults over 60, risks include smoking, diabetes, and UV exposure. Treatment requires a safe, 15-30 minute outpatient surgery to replace the cloudy lens with an artificial one, typically allowing quick recovery.

The main cause of cataracts is aging, as proteins in the eye's lens break down and clump together, causing clouding, but other major factors include long-term UV light exposure, smoking, diabetes, eye injuries, and steroid medication use. These risk factors accelerate the natural aging process, leading to vision becoming hazy or cloudy over time.

Summary

A cataract is a clouding of the lens of the eye, which is typically clear. For people who have cataracts, seeing through cloudy lenses is like looking through a frosty or fogged-up window. Clouded vision caused by cataracts can make it more difficult to read, drive a car at night or see the expression on a friend's face.

Most cataracts develop slowly and don't disturb eyesight early on. But with time, cataracts will eventually affect vision.

At first, stronger lighting and eyeglasses can help deal with cataracts. But if impaired vision affects usual activities, cataract surgery might be needed. Fortunately, cataract surgery is generally a safe, effective procedure.

Symptoms

Symptoms of cataracts include:

* Clouded, blurred or dim vision.
* Trouble seeing at night.
* Sensitivity to light and glare.
* Need for brighter light for reading and other activities.
* Seeing "halos" around lights.
* Frequent changes in eyeglass or contact lens prescription.
* Fading or yellowing of colors.
* Double vision in one eye.

At first, the cloudiness in your vision caused by a cataract may affect only a small part of the eye's lens. You may not notice any vision loss. As the cataract grows larger, it clouds more of your lens. More clouding changes the light passing through the lens. This may lead to symptoms you notice more.

When to see a doctor

Make an appointment for an eye exam if you notice any changes in your vision. If you develop sudden vision changes, such as double vision or flashes of light, sudden eye pain, or a sudden headache, see a member of your health care team right away.

Details

A cataract is a cloudy area in the lens of the eye that impairs vision. Cataracts often develop slowly and can affect one or both eyes. Symptoms may include faded colours, blurry or double vision, halos around light, trouble with bright lights, and difficulty seeing at night. This may result in difficulty driving, reading and recognizing faces. Poor vision caused by cataracts may also result in an increased risk of falling and depression. In 2020 Cataracts caused 39.6% of all cases of blindness and 28.3% of visual impairment worldwide. Cataracts remain the single most common cause of global blindness.

Cataracts are most commonly due to aging but may also be due to trauma or radiation exposure, be present from birth or occur following eye surgery for other problems. Risk factors include diabetes, longstanding use of corticosteroid medication, smoking tobacco, prolonged exposure to sunlight and alcohol. In addition, poor nutrition, obesity, chronic kidney disease and autoimmune diseases have been recognized in various studies as contributing to the development of cataracts. Cataract formation is primarily driven by oxidative stress, which damages lens proteins, leading to their aggregation and the accumulation of clumps of protein or yellow-brown pigment in the lens. This reduces the transmission of light to the retina at the back of the eye, impairing vision. Additionally, alterations in the lens's metabolic processes, including imbalances in calcium and other ions, contribute to cataract development. Diagnosis is typically through an eye examination, with ophthalmoscopy and slit-lamp examination being the most effective methods. During ophthalmoscopy the pupil is dilated and the red reflex is examined for any opacities in the lens. Slit-lamp examination provides further details on the characteristics, location and extent of the cataract.

Wearing sunglasses with UV protection and a wide brimmed hat, eating leafy vegetables and fruits and avoiding smoking may reduce the risk of developing cataracts or slow the process. Early on, the symptoms may be improved with glasses. If this does not help, surgery to remove the cloudy lens and replace it with an artificial lens is the only effective treatment. Cataract surgery is not readily available in many countries, and surgery is needed only if the cataracts are causing problems and generally results in an improved quality of life.

About 20 million people worldwide are blind owing to cataracts. They are the cause of approximately 5% of blindness in the United States and nearly 60% of blindness in parts of Africa and South America. Blindness from cataracts occurs in 10 to 40 per 100,000 children in the developing world and 1 to 4 per 100,000 children in the developed world. Cataracts become more common with age. In the United States, cataracts occur in 68% of those over the age of 80 years. They are more common in women and less common in Hispanic and Black people.

Additional Information

A cataract is a cloudy or opaque area in the normally clear lens of the eye. Depending upon its size and location, it can interfere with normal vision.

Most cataracts develop in people over age 55, but they occasionally occur in infants and young children or as a result of trauma or medications. Usually, cataracts develop in both eyes, but one may be worse than the other.

The lens is located inside the eye behind the iris, the colored part of the eye. Normally, the lens focuses light on the retina, which sends the image through the optic nerve to the brain. However, if the lens is clouded by a cataract, light is scattered so the lens can no longer focus it properly, causing vision problems. The lens is made of mostly proteins and water. The clouding of the lens occurs due to changes in the proteins and lens fibers.

Types of cataracts

The lens is composed of layers, like an onion. The outermost is the capsule. The layer inside the capsule is the cortex, and the innermost layer is the nucleus. A cataract may develop in any of these areas. Cataracts are named for their location in the lens:

* A nuclear cataract is located in the center of the lens. The nucleus tends to darken with age, changing from clear to yellow and sometimes brown.
* A cortical cataract affects the layer of the lens surrounding the nucleus. The cataract looks like a wedge or a spoke.
* A posterior capsular cataract is found in the back outer layer of the lens. This type often develops more rapidly.

Causes & risk factors

Most cataracts are due to age-related changes in the lens of the eye that cause it to become cloudy or opaque. However, other factors can contribute to cataract development, including:

* Diabetes mellitus. People with diabetes are at higher risk for cataracts.
* Drugs. Certain medications are associated with cataract development. These include:
** Corticosteroids.
** Chlorpromazine and other phenothiazine related medications.
* Ultraviolet radiation. Studies show an increased chance of cataract formation with unprotected exposure to ultraviolet (UV) radiation.
* Smoking. There is possibly an association between smoking and increased lens cloudiness.
* Alcohol. Several studies show increased cataract formation in patients with higher alcohol consumption compared with people who have lower or no alcohol consumption.
* Nutritional deficiency. Although the results are inconclusive, studies suggest an association between cataract formation and low levels of antioxidants (for example, vitamin C, vitamin E, and carotenoids). Further studies may show that antioxidants can help decrease cataract development.
* Family History. If a close relative has had cataracts, there is a higher chance of developing a cataract.

Rarely, cataracts are present at birth or develop shortly after. They may be inherited or develop due to an infection (such as rubella) in the mother during pregnancy. A cataract may also develop following an eye injury or surgery for another eye problem, such as glaucoma.

Symptoms

Cataracts generally form very slowly. Signs and symptoms of a cataract may include:

* Blurred or hazy vision.
* Reduced-intensity of colors.
* Increased sensitivity to glare from lights, particularly when driving at night.
* Increased difficulty seeing at night.
* Change in the eye's refractive error, or eyeglass prescription.

Diagnosis

Cataracts are diagnosed through a comprehensive eye examination. This examination may include:

* Patient history to determine if vision difficulties are limiting daily activities and other general health concerns affecting vision.
* Visual acuity measurement to determine to what extent a cataract may be limiting clear distance and near vision.
* Refraction to determine the need for changes in an eyeglass or contact lens prescription.
* Evaluation of the lens under high magnification and illumination to determine the extent and location of any cataracts.
* Evaluation of the retina of the eye through a dilated pupil.
* Measurement of pressure within the eye.
* Supplemental testing for color vision and glare sensitivity.

Further testing may be needed to determine how much the cataract is affecting vision and to evaluate whether other eye diseases may limit vision following cataract surgery.

Using the information from these tests, your doctor of optometry can determine if you have cataracts and advise you on your treatment options.

Treatment

Cataract treatment is based on the level of visual impairment they cause. If a cataract minimally affects vision, or not at all, no treatment may be needed. Patients may be advised to monitor for increased visual symptoms and follow a regular check-up schedule.

In some cases, changing the eyeglass prescription may provide temporary vision improvement. In addition, anti-glare coatings on eyeglass lenses can help reduce glare for night driving. Increasing the amount of light used when reading may be beneficial.

When a cataract progresses to the point that it affects a person's ability to do normal everyday tasks, surgery may be needed. Cataract surgery involves removing the lens of the eye and replacing it with an artificial lens. The artificial lens requires no care and can significantly improve vision. Some artificial lenses have the natural focusing ability of a young healthy lens. Once a cataract is removed, it cannot grow back.

Two approaches to cataract surgery are generally used:

* Small-incision cataract surgery involves making an incision in the side of the cornea (the clear outer covering of the eye) and inserting a tiny probe into the eye. The probe emits ultrasound waves that soften and break up the lens so it can be suctioned out. This process is called phacoemulsification.
* Extracapsular surgery requires a somewhat larger incision in the cornea so that the lens core can be removed in one piece. The natural lens is replaced by a clear plastic lens called an intraocular lens (IOL). When implanting an IOL is not possible because of other eye problems, contact lenses and, in some cases, eyeglasses may be an option for vision correction.

As with any surgery, cataract surgery has risks from infection and bleeding. Cataract surgery also slightly increases the risk of retinal detachment. It is important to discuss the benefits and risks of cataract surgery with your eye care providers. Other eye conditions may increase the need for cataract surgery or prevent a person from being a cataract surgery candidate.

Cataract surgery is one of the safest and most effective types of surgery performed in the United States today. Approximately 90% of cataract surgery patients report better vision following the surgery.

Prevention

There is no treatment to prevent or slow cataract progression. In age-related cataracts, changes in vision can be very gradual. Some people may not initially recognize the visual changes. However, as cataracts worsen, vision symptoms increase.

While there are no clinically proven approaches to preventing cataracts, simple preventive strategies include:

* Reducing exposure to sunlight through UV-blocking lenses.
* Decreasing or stopping smoking.
* Increasing antioxidant vitamin consumption by eating more leafy green vegetables and taking nutritional supplements.

Researchers have linked eye-friendly nutrients such as lutein and zeaxanthin, vitamin C, vitamin E and zinc to reducing the risk of certain eye diseases, including cataracts. For more information on the importance of good nutrition and eye health, please see the diet and nutrition section.

Jai Ganesh · Jai Ganesh's Puzzles

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#10783. What does the term in Geography Demilitarized zone mean?

#10784. What does the term in Geography Demography mean?

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#5979. What does the noun nesting mean?

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#2586. What does the medical term Endovascular aneurysm repair (EVAR) mean?

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Jai Ganesh · Exercises

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Jai Ganesh · This is Cool

2512) Intraocular Lens

Gist

Intraocular lenses (IOLs) are tiny, artificial, permanent lenses implanted inside the eye to replace a natural lens removed during cataract surgery or to correct refractive errors like myopia, hyperopia, and astigmatism. Made of acrylic or silicone, they restore clear vision by focusing light on the retina without needing maintenance.

Intraocular lenses usually last a lifetime. How is an intraocular lens used in cataract surgery? Cataract surgery involves removing the eye's natural lens which has become cloudy (cataract) and replacing it with an intraocular lens.

Summary

An intraocular lens (or IOL) is a tiny, artificial lens for the eye. It replaces the eye's natural lens that is removed during cataract surgery.

The lens bends (refracts) light rays that enter the eye, helping you to see. Your lens should be clear. But if you have a cataract, your lens has become cloudy. Things look blurry, hazy or less colorful with a cataract. Cataract surgery removes this cloudy lens and replaces it with a clear IOL to improve your vision.

IOLs come in different focusing powers, just like prescription eyeglasses or contact lenses. Your ophthalmologist will measure the length of your eye and the curve of your cornea. These measurements are used to set your IOLs focusing power.

What are IOLs made of?

Most IOLs are made of silicone, acrylic, or other plastic compositions. They are also coated with a special material to help protect your eyes from the sun's harmful ultraviolet (UV) rays.

Monofocal IOLs

The most common type of lens used with cataract surgery is called a monofocal IOL. It has one focusing distance. It is set to focus for up close, medium range or distance vision. Most people have them set for clear distance vision. Then they wear eyeglasses for reading or close work.

Some IOLs have different focusing powers within the same lens. These are called presbyopia-correcting IOLs. These IOLs reduce your dependence on glasses by giving you clear vision for more than one set distance.

Multifocal IOLs

These IOLs provide both distance and near focus at the same time. The lens has different zones set at different powers.

Extended depth-of-focus IOLs:

Similar to multifocal lenses, extended depth-of-focus (EDOF) lenses sharpen near and far vision, but with only one corrective zone, which “extends” to cover both distances. This may mean less effort to re-focus between distances.

Accommodative IOLs

These lenses move or change shape inside your eye, allowing focusing at different distances.

Toric IOLs

For people with astigmatism, there is an IOL called a toric lens. Astigmatism is a refractive error caused by an uneven curve in your cornea or lens. The toric lens is designed to correct that refractive error.

Details

An intraocular lens (IOL) is a lens implanted in the eye usually as part of a treatment for cataracts or for correcting other vision problems such as near-sightedness (myopia) and far-sightedness (hyperopia); a form of refractive surgery. If the natural lens is left in the eye, the IOL is known as phakic, otherwise it is a pseudophakic lens (or false lens). Both kinds of IOLs are designed to provide the same light-focusing function as the natural crystalline lens. This can be an alternative to LASIK, but LASIK is not an alternative to an IOL for treatment of cataracts.

IOLs usually consist of a small plastic lens with plastic side struts, called haptics, to hold the lens in place in the capsular bag inside the eye. IOLs were originally made of a rigid material (PMMA), although this has largely been superseded by the use of flexible materials, such as silicone. Most IOLs fitted today are fixed monofocal lenses matched to distance vision. However, other types are available, such as a multifocal intraocular lens that provides multiple-focused vision at far and reading distance, and adaptive IOLs that provide limited visual accommodation. Multifocal IOLs can also be trifocal IOLs or extended depth of focus (EDOF) lenses.

As of 2021, nearly 28 million cataract procedures took place annually worldwide. That is about 75,000 procedures per day globally. The procedure can be done under local or topical anesthesia with the patient awake throughout the operation. The use of a flexible IOL enables the lens to be rolled for insertion into the capsular bag through a very small incision, thus avoiding the need for stitches. This procedure usually takes less than 30 minutes in the hands of an experienced ophthalmologist, and the recovery period is about two to three weeks. After surgery, patients should avoid strenuous exercise or anything else that significantly increases blood pressure. They should visit their ophthalmologists regularly for three weeks to monitor the implants.

IOL implantation carries several risks associated with eye surgeries, such as infection, loosening of the lens, lens rotation, inflammation, nighttime halos and retinal detachment. Though IOLs enable many patients to have reduced dependence on glasses, most patients still rely on glasses for certain activities, such as reading. These reading glasses may be avoided in some cases if multifocal IOLs, trifocal IOLs or EDOF lenses are used.

Additional Information

IOLs (intraocular lenses) are clear, artificial lenses that replace your eye’s natural ones. You receive IOLs during cataract surgery and refractive lens exchange. IOL implants correct a range of vision issues, including nearsightedness and age-related farsightedness. They may also help reduce your reliance on glasses for certain types of tasks.

What are IOLs?

IOLs (intraocular lenses) are clear artificial lenses that a healthcare provider will implant in your eye to replace your natural lens. Like glasses or contacts, IOL implants can correct vision issues such as:

* Myopia (nearsightedness).
* Hyperopia (farsightedness).
* Presbyopia (age-related farsightedness).
* Astigmatism (altered eye shape).

IOL implants are permanent, meaning they stay in your eyes for the rest of your life. IOLs help improve your vision and may reduce your reliance on glasses in your daily routine. You receive IOLs during eye lens replacement surgery, most commonly during cataract surgery.

Who needs intraocular lens implants?

You may benefit from IOL implants if you:

* Have cataracts that prevent you from seeing clearly. Virtually everyone undergoing cataract surgery will need to have an IOL implant in order to restore vision.
* Have refractive errors that affect your vision, but you’re not a candidate for LASIK or other vision correction surgeries.

What are the different types of intraocular lenses?

There are many types of IOLs, each with its own pros and cons. The main drawback with some types of IOLs is you’ll still need to wear glasses for some tasks (like reading). Some IOLs can reduce your reliance on glasses, but you may notice side effects like glare around lights at night.

The list below covers some general categories of IOLs. Ask your ophthalmologist about which type of IOL is best for you. They’ll help you customize your IOL selection to suit your vision needs, lifestyle and personal preferences.

Monofocal lenses

This is the type of IOL that most people select. Monofocal lenses have one focusing power. This means they sharpen either your distance, mid-range or close-up vision. Most people set their monofocal lenses for distance vision, which can help with tasks like driving. You’ll probably still need glasses for close-up vision.

Monofocal lenses with monovision

Monofocal IOLs set to monovision are a good option for some people who want to rely less on glasses. Normally, the monofocal IOLs for both of your eyes are set to the same range (like distance). But with monovision, the lens for each eye has a different focusing power. For example, the lens for your right eye might correct for distance, with the lens for your left eye correcting for close-up vision.

With monovision, your eyes work together to help you see both distant and close-up objects. One drawback is that it takes some time to adapt to monovision. Some people can’t adapt to monovision at all. So, before choosing monovision IOLs, your provider may suggest you try monovision contact lenses for a couple of weeks. This allows you to see if this method of correction feels comfortable to you.

Multifocal lenses

Multifocal lenses improve your close-up and distance vision and may reduce your need for glasses. Unlike monofocal lenses, multifocal lenses contain several focal zones. Your brain adjusts to these zones and chooses the focusing power you need for any given task (like driving or reading). You may need some time to adapt to these lenses. But over time, you should be able to rely less on your reading glasses. Some people don’t need glasses at all.

One drawback of multifocal lenses is that you may notice rings or halos around lights, like when driving at night.

Extended depth-of-focus (EDOF) lenses

Unlike multifocal lenses, EDOF lenses contain one long focal point that expands your corrected range of vision and depth of focus. These lenses give you excellent distance vision along with improvements in your mid-range vision (for tasks such as computer use). You may still need to use glasses for close-up tasks like reading.

Accommodative lenses

These lenses are similar to your eyes’ natural lenses in that they adjust their shape to help you see close-up or distant objects. Accommodative lenses are another option to help reduce dependency on glasses. But you may prefer to use glasses if you’re reading or focusing on close-up objects for longer periods of time.

Toric lenses

Toric lenses help people who have astigmatism. These lenses improve how light hits your retina, allowing you to have a sharper, clearer vision. Toric lenses are available in monofocal, multifocal, extended depth of focus (EDOF) or accommodative models. They serve to improve the quality of the vision delivered. Toric lenses will help reduce the amount of glare and halos artifacts commonly experienced by people with astigmatism.

Light-adjustable lenses (LALs)

Light-adjustable lenses are different from other IOL options in that your ophthalmologist fine-tunes their corrective power after your lens replacement surgery. They do this through a series of UV light treatment procedures, spaced several days apart. These procedures customize your lens prescription to bring you as close to your desired visual outcome as possible. This is still a type of monofocal lens, so glasses will be necessary for reading or driving.

Phakic lenses

Phakic lenses are typically implanted in younger individuals while trying to preserve the natural human lens, to correct for near-sightedness in people who don’t qualify for laser refractive surgery. This helps preserve your natural ability to focus and accommodate. These lenses will eventually have to be removed during cataract surgery but can offer younger people clear vision for a long time.

Which intraocular lens is best for me?

Your ophthalmologist will determine if you would benefit from cataract surgery, or if you would qualify for a refractive lens exchange surgery. They’ll discuss your options and help you decide which IOLs are best for you. They’ll also conduct a thorough eye exam to check your vision and the health of your eyes. They’ll perform some simple, painless tests to measure your eye size and shape, too.

To prepare for a conversation with your ophthalmologist, you should think about your priorities for your IOLs, as well as aspects that aren’t as important to you. It may help to ask yourself the following questions:

* Am I OK wearing glasses sometimes? If so, how often and for what types of tasks?
* What kind of vision is required in my work/profession? Am I OK wearing glasses for these tasks?
* Do I drive often at night? If so, can I adapt to seeing glare and halos around lights when I drive?
* What kind of hobbies and activities do I enjoy the most and how much dependency on glasses am I OK with for these activities?
* What is my budget for surgery?

Most insurance plans cover monofocal lenses, but you may have to pay for other types out of pocket. Be sure to find out the cost of various IOL options before making your final decision.

What are possible issues and complications related to IOL implantation?

Most IOL complications are rare and include:

* Posterior capsular opacification:This is commonly known as a secondary cataract. This happens after many months or years when a film-like material grows behind the implanted lens. This is a normal process that happens after surgery and can be expected to occur over time for almost everyone. The treatment for this is very quick and straightforward and is usually performed using a laser in the office.
* IOL dislocation: This means your IOL shifts from its normal position. You face a higher risk if you have certain eye conditions, like pseudoexfoliation syndrome, or have had trauma or prior eye surgeries. Certain genetic disorders, such as Ehlers-Danlos syndrome and Marfan syndrome, may also raise your risk. In some cases, you may need surgery to reposition or replace the IOL.
* Uveitis-glaucoma-hyphema (UGH) syndrome: UGH syndrome occurs when an IOL irritates your iris and other parts of your eye. This leads to inflammation, raised intraocular pressure and other symptoms. As with IOL dislocation, you may need surgery to reposition or replace the IOL. This is an extremely rare complication that most people don’t experience with routine surgery.
* IOL opacification: This is a clouding of your IOL. Your vision may become less sharp, and you may notice glare around lights. Treatment involves surgery to give you a new IOL. This is extremely uncommon with modern-day IOLs.
* Refractive surprise: A refractive surprise is when your vision after IOL implantation isn’t as sharp as you and your ophthalmologist expected. Your ophthalmologist will suggest a range of solutions. You may decide to accept the vision correction as is and do nothing further. Or you can choose to wear glasses, have laser vision correction (such as LASIK or PRK) or have an IOL replacement surgery.

Talk with your ophthalmologist about possible complications and your level of risk before choosing to have IOLs implanted in your eyes. They’ll tell you what to expect based on your medical history, eye health and other factors. Also, ask them about common side effects associated with cataract surgery or refractive lens exchange. Be sure to get all the information you need to make the decision that’s right for you.

LASIK

LASIK is a laser eye surgery that corrects vision problems. It changes the shape of your cornea to improve how light hits your retina. This improves your vision. About 99% of people have uncorrected vision that’s 20/40 or better after their LASIK surgery. More than 90% end up with 20/20 vision. Dry eye is the most common side effect.

PRK

Photorefractive keratectomy (PRK) is a laser eye surgery similar to LASIK. Unlike LASIK, which involves opening a flap in your cornea, PRK removes your cornea so that it grows back naturally. That makes it a better laser eye surgery choice for some people who can’t undergo LASIK.

Jai Ganesh · Dark Discussions at Cafe Infinity

2449) Walther Bothe

Gist:

Work

In a counter tube, particles passing through the tube generate an electric pulse. In 1925 Walter Bothe connected two counter tubes together so that only simultaneous passages were registered. This meant that either the passages were caused by particles that originated from the same event or by a particle that moved so fast that the time for movement between the tubes was negligible. Bothe used the method to show that energy is conserved in impacts between particles and photons and to study cosmic radiation.

Summary

Walther Bothe (born Jan. 8, 1891, Oranienburg, Ger.—died Feb. 8, 1957, Heidelberg, W.Ger.) was a German physicist who shared the Nobel Prize for Physics in 1954 with Max Born for his invention of a new method of detecting subatomic particles and for other resulting discoveries.

Bothe taught at the universities of Berlin (1920–31), Giessen (1931–34), and Heidelberg (1934–57). In 1925 he and Hans Geiger used two Geiger counters to gather data on the Compton effect—the dependence of the increase in the wavelength of a beam of X rays upon the angle through which the beam is scattered as a result of collision with electrons. Their experiments, which simultaneously measured the energies and directions of single photons and electrons emerging from individual collisions, refuted a statistical interpretation of the Compton effect and definitely established the particle nature of electromagnetic radiation.

With the astronomer Werner Kolhörster, Bothe again applied this coincidence-counting method in 1929 and found that cosmic rays are not composed exclusively of gamma rays, as was previously believed. In 1930 Bothe discovered an unusual radiation emitted by beryllium when it is bombarded with alpha particles. This radiation was later identified by Sir James Chadwick as the neutron.

During World War II Bothe was one of the leaders of German research on nuclear energy. He was responsible for the planning and building of Germany’s first cyclotron, which was completed in 1943.

Details

Walther Wilhelm Georg Bothe (8 January 1891 – 8 February 1957) was a German experimental physicist who shared the 1954 Nobel Prize in Physics with Max Born "for the coincidence method and his discoveries made therewith."

Bothe served in the military during World War I from 1914, and he was a prisoner of war of the Russians, returning to Germany in 1920. Upon his return to the laboratory, he developed and applied coincidence circuits to the study of nuclear reactions, such as the Compton effect, cosmic rays, and the wave–particle duality of radiation.

In 1930, Bothe became Full Professor and Director of the Physics Department at the University of Giessen. In 1932, he became Director of the Physical and Radiological Institute at the University of Heidelberg; he was driven out of this position by elements of the Deutsche Physik movement. To preclude his emigration from Germany, he was appointed Director of the Physics Institute of the Kaiser Wilhelm Institute for Medical Research in Heidelberg. There, he built the first operational cyclotron in Germany. Furthermore, he became a principal in the German nuclear energy project, also known as Uranverein, which was started in 1939 under the supervision of the Army Ordnance Office.

In 1946, in addition to his directorship of the Physics Institute at the KWImf, Bothe was reinstated as a professor at the University of Heidelberg. From 1956 to 1957, he was a member of the Nuclear Physics Working Group in Germany.

In the year after Bothe's death, his Physics Institute at the KWImF was elevated to the status of a new institute under the Max Planck Society and it then became the Max Planck Institute for Nuclear Physics. Its main building was later named Bothe laboratory.

Education

Walther Wilhelm Georg Bothe was born on 8 January 1891 in Oranienburg, Germany, the son of Friedrich Bothe and Charlotte Hartung.

From 1908 to 1912, Bothe studied at the University of Berlin. In 1913, he became Max Planck's teaching assistant. He received his Ph.D. under Planck the following year.

Jai Ganesh · Jokes

Q: Why didn't the obese man know he was overweight?
A: Because it kinda just snacked up on him!
* * *
Q: Why are all obese Americans actually in shape?
A: Because the shape is a triangle!
* * *
Q: What did the plate say to the other plate?
A: Dinners on me tonight.
* * *
Q: What happened to the snack bar that was too close to the Atom Smasher?
A: They created "Fission chips".
* * *
Q: What kind of candy is never on time?
A: ChocoLATE.
* * *

Jai Ganesh · Dark Discussions at Cafe Infinity

Come Quotes - XXI

1. When we look back on all the perils through which we have passed and at the mighty foes that we have laid low and all the dark and deadly designs that we have frustrated, why should we fear for our future? We have come safely through the worst. - Winston Churchill

2. Whether you come from a council estate or a country estate, your success will be determined by your own confidence and fortitude. - Michelle Obama

3. The smaller the planets are, they are, other things being equal, of so much the greater density; for so the powers of gravity on their several surfaces come nearer to equality. They are likewise, other things being equal, of the greater density, as they are nearer to the sun. - Isaac Newton

4. If you want to cut your own throat, don't come to me for a bandage. - Margaret Thatcher

5. I've been here before and will come again, but I'm not going this trip through. - Bob Marley

6. I perhaps ought to say that individually I never was much interested in the Texas question. I never could see much good to come of annexation, inasmuch as they were already a free republican people on our own model. - Abraham Lincoln

7. This is the moment when we must come together to save this planet. Let us resolve that we will not leave our children a world where the oceans rise and famine spreads and terrible storms devastate our lands. - Barack Obama

8. We will burn that bridge when we come to it. - Johann Wolfgang von Goethe.

Jai Ganesh · This is Cool

Mountain K2

Gist

K2 is the world's second-highest mountain at 8,611 meters (28,251 ft), located on the China-Pakistan border in the Karakoram Range. Known as the "Savage Mountain" for its extreme, unpredictable weather and treacherous terrain, it is considered one of the most difficult and dangerous peaks to climb.

K2 is harder than Everest because it's much more technically challenging with steeper, icy faces, unpredictable and brutal weather (more wind, sudden storms), and greater remoteness, offering fewer rescue options, leading to a significantly higher fatality rate despite being slightly shorter than Everest. Everest has more established routes and support, while K2 demands pure skill with little room for error, earning it nicknames like "Savage Mountain".

Summary

K2 is the world’s second highest peak (28,251 feet [8,611 metres]), second only to Mount Everest. K2 is located in the Karakoram Range and lies partly in a Chinese-administered enclave of the Kashmir region within the Uygur Autonomous Region of Xinjiang, China, and partly in the Gilgit-Baltistan portion of Kashmir under the administration of Pakistan.

The glacier- and snow-covered mountain rises from its base at about 15,000 feet (4,570 metres) on the Godwin Austen Glacier, a tributary of the Baltoro Glacier. The mountain was discovered in 1856 by Col. T.G. Montgomerie of the Survey of India, and it was given the symbol K2 because it was the second peak measured in the Karakoram Range. The name Mount Godwin Austen is for the peak’s first surveyor, Col. H.H. Godwin Austen, a 19th-century English geographer.

The first attempt to reach the summit was made by an Anglo-Swiss expedition in 1902 that ascended to 18,600 feet (5,670 metres) on the peak’s northeastern crest. Other unsuccessful attempts included an Italian expedition in 1909, led by Luigi Amedeo, duke d’Abruzzi, via the southeastern ridge (later called the Abruzzi Ridge) that reached approximately 20,000 feet (6,100 metres). In 1938 an American expedition led by Charles Houston via the Abruzzi Ridge reached about 26,000 feet (7,925 metres); in 1939 another American-led expedition following the same route reached about 27,500 feet (8,380 metres); and in 1953 another expedition led by Houston reached 25,900 feet (7,900 metres) on the Abruzzi Ridge. Finally, in 1954, an Italian expedition consisting of five scientists (including the geologist Ardito Desio as leader), a doctor, a photographer, and 12 others, including a Pakistani, managed to conquer the Abruzzi Ridge despite the severe weather conditions. The summit was reached at 6 pm on July 31, 1954, by Achille Compagnoni and Lino Lacedelli. In the course of the ascent, Mario Puchoz, one of the guides, died of pneumonia.

Because K2 is prone to frequent and severe storms that make the already treacherous climbing conditions on its slopes even more challenging—and humans find functioning at such high elevations difficult—it is one of the world’s most difficult mountains to climb. The number of people to have reached the top constitutes only a small fraction compared with how many have successfully climbed Mount Everest. In addition, although there have been fewer deaths on K2 compared with those on Mount Everest, the proportion of those killed to the number of people who have attempted climbing K2 is significantly higher.

Details

K2, also known as Mount Godwin-Austen, at 8,611 metres (28,251 ft) above sea level, is the second-highest mountain on Earth, after Mount Everest at 8,849 metres (29,032 ft). It lies in the Karakoram range, partially in the Gilgit-Baltistan region of Pakistan-administered Kashmir and partially in the China-administered Trans-Karakoram Tract in the Taxkorgan Tajik Autonomous County of Xinjiang.

K2 became known as the Savage Mountain after George Bell—a climber on the 1953 American expedition—said, "It's a savage mountain that tries to kill you." Of the five highest mountains in the world, K2 has long been the deadliest: prior to 2021, approximately one person had died on the mountain for every four who reached the summit. After an increase in successful attempts, as of August 2023, an estimated 800 people have summited K2, with 96 deaths during attempted climbs.

K2 is nicknamed "The King of Mountains" and "The Mountaineers' Mountain", as well as "The Mountain of Mountains", a phrase popularized by Italian climber Reinhold Messner in his book on K2. Although the summit of Everest is at a higher altitude, K2 is a more difficult and dangerous climb. This is in part due to its more northern location, where inclement weather is more common, as well as its steep and exposed faces. The summit was reached for the first time by the Italian climbers Lino Lacedelli and Achille Compagnoni on a 1954 Italian expedition led by Ardito Desio.

Most ascents are made during July and August, typically the warmest times of the year. In January 2021 K2 became the final eight-thousander to be summited in the winter by a team of Nepalese climbers led by Nirmal Purja and Mingma Gyalje Sherpa.

K2's eastern face remains un-climbed, partly because of the hazards associated with the instability of its ice and snow formations.

Geographical setting

K2 lies in the northwestern Karakoram Range. It is located in the Baltistan region of Gilgit–Baltistan, Pakistan, and the Taxkorgan Tajik Autonomous County of Xinjiang, China. The Tarim sedimentary basin borders the range on the north and the Lesser Himalayas on the south. Melt waters from glaciers, such as those south and east of K2, feed agriculture in the valleys and contribute significantly to the regional fresh-water supply.

K2 is ranked 22nd by topographic prominence, a measure of a mountain's independent stature. It is a part of the same extended area of uplift (including the Karakoram, the Tibetan Plateau, and the Himalayas) as Mount Everest, and it is possible to follow a path from K2 to Everest that goes no lower than 4,594 metres (15,072 ft), at the Kora La on the Nepal/China border in the Mustang Lo. Many other peaks far lower than K2 are more independent in this sense. It is, however, the most prominent peak within the Karakoram range.

K2 is notable for its local relief as well as its total height. It stands over 3,000 metres (10,000 ft) above much of the glacial valley bottoms at its base. It is a consistently steep pyramid, dropping quickly in almost all directions. The north side is the steepest: there it rises over 3,200 metres (10,500 ft) above the K2 (Qogir) Glacier in only 3,000 metres (9,800 ft) of horizontal distance. In most directions, it achieves over 2,800 metres (9,200 ft) of vertical relief in less than 4,000 metres (13,000 ft).

A 1986 expedition led by George Wallerstein made an inaccurate measurement showing that K2 was taller than Mount Everest, and therefore the tallest mountain on Earth. A corrected measurement was made in 1987, but by then the claim that K2 was the tallest mountain in the world had already made it into many news reports and reference works.

Height

K2's height given on maps and encyclopedias is 8,611 metres (28,251 ft). In the summer of 2014, a Pakistani-Italian expedition to K2, named "K2 60 Years Later", was organized to commemorate the 60th anniversary of the first ascent of K2. One of the goals of the expedition was to accurately measure the height of the mountain using satellite navigation. The height of K2 measured during this expedition was 8,609.02 metres (28,244.8 ft).

Additional Information

K2 is the second-highest mountain in the world, standing at 8,611 metres (28,251 ft) tall. It is also known as Mount Godwin-Austen or Chogori. K2 is part of the Karakoram mountain range, and is located on the border between Pakistan and China. The name, 'K2' originated from the first survey of the Karakoram range. In the survey, surveyors named each mountain with a 'K' and a number after that.

K2 is known as the 'Savage Mountain' and is considered more difficult to climb than Mount Everest,which is the highest mountain in the world. It has the second-highest fatality rate among all mountains.With a height over 8,000 meters, with a rate of approximately one death for every four climbers who reach the summit. As of 2011, only 300 people had successfully reached the top of K2, while more than 80 climbers lost their lives attempting the ascent. K2 can be climbed during both summer and winter seasons.

The top of the mountain was first reached in 1954 by Italian climbers Lino Lacedelli and Achille Compagnoni.

Mount K2, the second-highest mountain on Earth (Mount Everest), is the world’s second-highest Mountain. Stands as a remote and terrifying sentinel in the Karakoram Range. Unlike Mt. Everest, it remains as off-the-beaten-path far from popular trekking circuits, demanding effort even to glimpse its icy crown. Located on the border between Pakistan and China, K2 rises to a height of 8,611 meters (28,251 feet) above sea level. It dominates the skyline of Pakistan’s Gilgit-Baltistan region, surrounded by glaciers, deep valleys, and other towering peaks.

Jai Ganesh · Science HQ

Fibula

Gist

The fibula (calf bone) is the slender, long bone located on the lateral (outer) side of the tibia in the lower leg. While it does not bear significant weight, it is crucial for stabilizing the ankle joint, supporting lower-leg muscles, and forming the lateral malleolus. It connects to the tibia via an interosseous membrane.

The fibula, or calf bone, is the slender, outer bone in the lower leg, running parallel to the larger shin bone (tibia) from just below the knee to the ankle, forming the bony bump (lateral malleolus) on the outside of your ankle and providing vital stability and muscle attachment for movement, though it's not a primary weight-bearing bone.

Summary

Fibula is the outer of two bones of the lower leg or hind limb, presumably so named (fibula is Latin for “brooch”) because the inner bone, the tibia, and the fibula together resemble an ancient brooch, or pin. In humans the head of the fibula is joined to the head of the tibia by ligaments and does not form part of the knee. The base of the fibula forms the outer projection (malleolus) of the ankle and is joined to the tibia and to one of the ankle bones, the talus. The tibia and fibula are further joined throughout their length by an interosseous membrane between the bones. The fibula is slim and roughly four-sided, and its shape varies with the strength of the attached muscles. In many mammals, such as the horse and the rabbit, the fibula is fused for part of its length with the tibia.

Fractures of the fibula usually are associated with an ankle injury, though they can occur in isolation (without ankle involvement) or in combination with fractures of the tibia (e.g., in severe injuries). Though less common that tibial stress fractures, fibular stress fractures can occur, most typically in long-distance runners.

Details

The fibula (pl.: fibulae or fibulas) or calf bone is a leg bone on the lateral side of the tibia, to which it is connected above and below. It is the smaller of the two bones and, in proportion to its length, the most slender of all the long bones. Its upper extremity is small, placed toward the back of the head of the tibia, below the knee joint and excluded from the formation of this joint. Its lower extremity inclines a little forward, so as to be on a plane anterior to that of the upper end; it projects below the tibia and forms the lateral part of the ankle joint.

Structure

The bone has the following components:

* Lateral malleolus
* Interosseous membrane connecting the fibula to the tibia, forming a syndesmosis joint
* The superior tibiofibular articulation is an arthrodial joint between the lateral condyle of the tibia and the head of the fibula.
* The inferior tibiofibular articulation (tibiofibular syndesmosis) is formed by the rough, convex surface of the medial side of the lower end of the fibula, and a rough concave surface on the lateral side of the tibia.

Blood supply

The blood supply is important for planning free tissue transfer because the fibula is commonly used to reconstruct the mandible. The shaft is supplied in its middle third by a large nutrient vessel from the fibular artery. It is also perfused from its periosteum which receives many small branches from the fibular artery. The proximal head and the epiphysis are supplied by a branch of the anterior tibial artery. In harvesting the bone the middle third is always taken and the ends preserved (4 cm proximally and 6 cm distally)

Development

The fibula is ossified from three centers, one for the shaft, and one for either end. Ossification begins in the body about the eighth week of fetal life, and extends toward the extremities. At birth the ends are cartilaginous.

Ossification commences in the lower end in the second year, and in the upper about the fourth year. The lower epiphysis, the first to ossify, unites with the body about the twentieth year; the upper epiphysis joins about the twenty-fifth year.

Head

The upper extremity or head of the fibula is of an irregular quadrate form, presenting above a flattened articular surface, directed upward, forward, and medialward, for articulation with a corresponding surface on the lateral condyle of the tibia. On the lateral side is a thick and rough prominence continued behind into a pointed eminence, the apex (styloid process), which projects upward from the posterior part of the head.

The prominence, at its upper and lateral part, gives attachment to the tendon of the biceps femoris and to the fibular collateral ligament of the knee-joint, the ligament dividing the tendon into two parts.

The remaining part of the circumference of the head is rough, for the attachment of muscles and ligaments. It presents in front a tubercle for the origin of the upper and anterior fibers of the peroneus longus, and a surface for the attachment of the anterior ligament of the head; and behind, another tubercle, for the attachment of the posterior ligament of the head and the origin of the upper fibers of the soleus.

Body

The body of the fibula presents four borders - the antero-lateral, the antero-medial, the postero-lateral, and the postero-medial; and four surfaces - anterior, posterior, medial, and lateral.

Borders

The antero-lateral border begins above in front of the head, runs vertically downward to a little below the middle of the bone, and then curving somewhat lateralward, bifurcates so as to embrace a triangular subcutaneous surface immediately above the lateral malleolus. This border gives attachment to an intermuscular septum, which separates the extensor muscles on the anterior surface of the leg from the peronaei longus and brevis on the lateral surface.

The antero-medial border, or interosseous crest, is situated close to the medial side of the preceding, and runs nearly parallel with it in the upper third of its extent, but diverges from it in the lower two-thirds. It begins above just beneath the head of the bone (sometimes it is quite indistinct for about 2.5 cm. below the head), and ends at the apex of a rough triangular surface immediately above the articular facet of the lateral malleolus. It serves for the attachment of the interosseous membrane, which separates the extensor muscles in front from the flexor muscles behind.

The postero-lateral border is prominent; it begins above at the apex, and ends below in the posterior border of the lateral malleolus. It is directed lateralward above, backward in the middle of its course, backward, and a little medialward below, and gives attachment to an aponeurosis which separates the peronaei on the lateral surface from the flexor muscles on the posterior surface.

The postero-medial border, sometimes called the oblique line, begins above at the medial side of the head, and ends by becoming continuous with the interosseous crest at the lower fourth of the bone. It is well-marked and prominent at the upper and middle parts of the bone. It gives attachment to an aponeurosis which separates the tibialis posterior from the soleus and flexor hallucis longus.

Surfaces

The anterior surface is the interval between the antero-lateral and antero-medial borders. It is extremely narrow and flat in the upper third of its extent; broader and grooved longitudinally in its lower third; it serves for the origin of three muscles: the extensor digitorum longus, extensor hallucis longus, and peroneus tertius.

The posterior surface is the space included between the postero-lateral and the postero-medial borders; it is continuous below with the triangular area above the articular surface of the lateral malleolus; it is directed backward above, backward and medialward at its middle, directly medialward below. Its upper third is rough, for the origin of the soleus; its lower part presents a triangular surface, connected to the tibia by a strong interosseous ligament; the intervening part of the surface is covered by the fibers of origin of the flexor hallucis longus. Near the middle of this surface is the nutrient foramen, which is directed downward.

The medial surface is the interval included between the antero-medial and the postero-medial borders. It is grooved for the origin of the tibialis posterior.

The lateral surface is the space between the antero-lateral and postero-lateral borders. It is broad, and often deeply grooved; it is directed lateralward in the upper two-thirds of its course, backward in the lower third, where it is continuous with the posterior border of the lateral malleolus. This surface gives origin to the peronaei longus and brevis.

Clinical significance

As much of the fibula can be removed without it impacting an individual's ability to walk, the fibula is utilised as a source of bone material in fibular free flap surgeries.

Fractures

The most common type of fibula fracture is located at the distal end of the bone, and is classified as ankle fracture. In the Danis–Weber classification it has three categories:

* Type A: Fracture of the lateral malleolus, distal to the syndesmosis (the connection between the distal ends of the tibia and fibula).
* Type B: Fracture of the fibula at the level of the syndesmosis
* Type C: Fracture of the fibula proximal to the syndesmosis.

A Maisonneuve fracture is a spiral fracture of the proximal third of the fibula associated with a tear of the distal tibiofibular syndesmosis and the interosseous membrane. There is an associated fracture of the medial malleolus or rupture of the deep deltoid ligament.

An avulsion fracture of the head of the fibula refers to the fracture of the fibular head because of a sudden contraction of the biceps femoris muscle that pulls its site of attachment on the bone. The attachment of the biceps femoris tendon on the fibular head is closely related to the lateral collateral ligament of the knee. Therefore, this ligament is prone to injury in this type of avulsion fracture.

Additional Information

The fibula is a slender, cylindrical leg bone that is located on the posterior portion of the limb. It is found next to another long bone known as the tibia. A long bone is defined as one whose body is longer than it is wide.

Like other long bones, the fibula has a proximal end (with a head and neck), a shaft, and a distal end. The fibula and tibia run parallel to each other in the leg and are similar in length but the fibula is much thinner than the tibia. This is indicative of the weight-bearing contributions of each bone. In other words, the thicker tibia has a much greater function in weight-bearing than the fibula.

There are several key facts about the fibula that most anatomy students should be familiar with. These and other important points about the anatomy, blood supply, innervation, and muscular and ligamentous attachments are addressed in this article. The article will also discuss important fractures of the fibula.

Development

The fibula is a part of the appendicular skeleton and develops via endochondral ossification. There are three points at which ossification begins in the fibula:

* the body around the 8th gestational week
* the distal end by the end of the first year of life
* the proximal end at around four-years-old in males and three-years-old in females

The ossification centers of the body and distal end of the bone eventually fuse during the mid-adolescent years (at 15 years old for females and 17 years old for males). The bony centers of the proximal part and shaft of the fibula are the last to unite during the late adolescent years (around 17 years for females and 19 years for males).

Proximal end

The proximal end of the fibula is characterized by an irregularly shaped head and a short neck. It has three segments which project in different directions: anteriorly, posteriorly, and laterally. An important question that pops up on a lot of anatomy tests is with what bony structure does the head of the fibula articulate? There is a round, flattened area on the medial part of the fibular head known as a facet. It articulates with a complementary facet on the inferolateral part of the lateral tibial condyle (proximal tibiofibular joint). The facet also acts as a point of attachment for the tibiofibular capsular ligament. Additionally, the tibiofibular capsular ligament surrounds the articular facet of the fibula.

There is a styloid process of the fibula that extends superiorly from the head; it is more commonly referred to as the apex of the head of the fibula. This apical projection protrudes from the posterolateral part of the fibular head. The neck of the fibula is a short bare region just below the fibular head. What important structures pass around the neck of the fibula? Importantly, the common fibular nerve (also called the common peroneal nerve) travels posterolaterally to the fibular neck. This has clinical significance as trauma to the neck of the fibula can present with neurological deficits.

The function of the proximal end of the fibula is to provide points of attachment for minor supporting ligaments of the knee joint. There is the fibular collateral ligament that arises from the fibular apex and is surrounded by the tendon of biceps femoris.

Body

The majority of the fibula is made up by its body (or shaft). This part of the bone is triangular in cross-section and consequently has three borders (anterior, interosseous, and posterior) and three surfaces (lateral, medial, and posterior) found along the shaft of the fibula. The borders are the sharp longitudinal edges that run along the bone’s long axis. On the other hand, the surfaces are the flattened areas that exist between the borders.

The anterior border starts at the fibular head and continues distally toward the lateral malleolus, where it diverges into two ridges that surround the triangular subcutaneous surface. On the medial aspect of the fibula is the interosseous or medial border. It is the point of attachment of the fibrous interosseous membrane of the leg that forms the middle tibiofibular joint. This fibrous septum acts as a barrier between the extensor and fibular muscles. There is a posterior border that runs along the back part of the fibula. The proximal part of the border appears slightly rounded. However, the border becomes more prominent distally, as it approaches the medial segment of the lateral malleolus.

The interosseous and anterior borders of the fibula act as medial and lateral boundaries of the medial surface. This surface provides a point of attachment for the muscles that extend the foot and cause the toes to point upward (dorsiflexion).

The lateral surface is found on the opposite side of the medial surface, between the posterior and anterior borders. The proximal part of the surface faces laterally; however, the surface spirals toward the distal end and as such part of the surface faces posterolaterally. By virtue of this shift, the distal part of the lateral surface is in continuity with the posterior groove of the lateral malleolus. The lateral surface provides a point of attachment for the fibular (peroneal) muscles.

The posterior surface is found between the posterior and interosseous borders. The surface is much more narrow at the proximal part (where the interosseous and posterior borders are closest) than it is distally (where the borders are farthest apart). This surface provides attachment for the flexor muscles of the foot which are responsible for pointing the toes downward (plantar flexion).

Distal end

The distal end of the fibula forms the lateral malleolus of the lower limb. This is a bony projection noted on the lateral surface of the ankle, which is complementary to another bony projection on the medial aspect of the ankle called the medial malleolus (formed by the tibia). The lateral malleolus extends posteroinferiorly, is round and rough anteriorly, and has a broad groove posteriorly. The lateral surface is covered by skin (so there is no muscular layer at this area) and the medial surface has a triangular area that is convex along the vertical axis. The distal end of the fibula tapers off as an apical projection that articulates with the lateral aspect of the talus.

The distal end provides attachment for several ligaments that support the ankle joint. The posterior tibiofibular, posterior talofibular, calcaneofibular, and interosseous (middle) tibiofibular ligaments all have attachments to the end of the fibula and participate in the stability of this joint.

Joints

The tibia and fibula articulate through three joints–the superior, middle, and inferior tibiofibular joints. The superior tibiofibular joint is a plane synovial joint (allows only gliding movement) with the transverse joint line spanning the lateral tibial condyle and the medial fibular head. The capsule is thickened anteriorly and posteriorly and joins with the anterior ligament of the fibular head, relating closely to the tendon of biceps femoris.

The tibia and fibula also articulate via an interosseous membrane that is also called the middle tibiofibular ligament. It is made of an aponeurotic lamina which is thin and made of oblique fibers. This ligament has medial and lateral attachments to the tibial and fibular interosseous margins respectively. The membrane separates the muscles in the back of the leg from the muscles located in the front of the leg.

The inferior tibiofibular joint is a syndesmosis joint (slightly movable, fibrous joint), just above the ankle region which lies between the medial distal end of the fibula and the concave fibular notch region of the lateral tibia. There is no fibrous capsule surrounding this joint but there is the anterior tibiofibular ligament which descends laterally between the two leg bones.

Muscle attachments

What is the function of the fibula? The bone provides a point of origin for a number of muscles of the foot. However, only one muscle inserts on this long bone. So what structures are attached to the fibula? The table below summarizes the muscles that originate from, and insert on the fibula. Note that the muscles are listed from cranial to caudal, and those attached to the anterior surface are listed before those on the posterior surface.

Blood supply and innervation

A branch of the fibular artery brings oxygen-rich blood to supply the bone. It travels through a nutrient foramen on the posterior surface of the fibula that facilitates passage of a branch of the fibular artery into the bone. The foramen is a few centimeters proximal to the midpoint of the shaft.

The nerves that supply the knee (genicular branch of the common fibular nerve) and ankle (deep fibular nerve) joints also innervate the proximal and distal ends of the fibula, respectively. Similarly, superficial and deep fibular nerves, which innervate the muscles attached to the fibula, also innervate the fibular periosteum.

Jai Ganesh · Jai Ganesh's Puzzles

Hi,

#10781. What does the term in Geography Dell (landform) mean?

#10782. What does the term in Geography River delta mean?

Jai Ganesh · Jai Ganesh's Puzzles

Hi,

#5977. What does the noun hallmark mean?

#5978. What does the adjective hallowed mean?

Jai Ganesh · Jai Ganesh's Puzzles

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2511) Tonometry

Gist

Tonometry is a quick, non-invasive diagnostic procedure that measures intraocular pressure (IOP), or fluid pressure inside the eye, to detect and monitor glaucoma. By assessing how much force is needed to flatten the cornea (applanation) or indent it, doctors can check for optic nerve damage. The most common methodGoldmann applanation tonometry, is considered the gold standard.

How is tonometry performed?

The lamp is moved forward until the tip of the tonometer just touches the cornea. Blue light is used so that the orange dye will glow green. The health care provider looks through the eyepiece on the slit-lamp and adjusts a dial on the machine to give the pressure reading. There is no discomfort with the test.

Summary

A tonometry test measures the pressure inside your eye, which is called intraocular pressure (IOP). This test is used to check for glaucoma, an eye disease that can cause blindness by damaging the nerve in the back of the eye (optic nerve). Damage to the optic nerve may be caused by a buildup of fluid that does not drain properly out of the eye.

Tonometry measures IOP by recording the resistance of your cornea to pressure (indentation). Eyedrops to numb the surface of your eye are used with most of the following methods.

Tonometry methods

* Applanation (Goldmann) tonometry. This type of tonometry uses a small probe to gently flatten part of your cornea to measure eye pressure and a microscope called a slit lamp to look at your eye. The pressure in your eye is measured by how much force is needed to flatten your cornea. This type of tonometry is very accurate and is often used to measure IOP after a simple screening test (such as air-puff tonometry) finds an increased IOP.
* Electronic indentation tonometry. Electronic tonometry is being used more often to check for increased IOP. Although it is very accurate, electronic tonometry results can be different than applanation tonometry. Your doctor gently places the rounded tip of a tool that looks like a pen directly on your cornea. The IOP reading shows on a small computer panel.
* Noncontact tonometry (pneumotonometry). Noncontact (or air-puff) tonometry does not touch your eye but uses a puff of air to flatten your cornea. This type of tonometry is not the best way to measure intraocular pressure. But it is often used as a simple way to check for high IOP and is the easiest way to test children. This type of tonometry does not use numbing eyedrops.

Details

Tonometry is a test to measure the pressure inside your eyes. The test is used to screen for glaucoma. It is also used to measure how well glaucoma treatment is working.

How the Test is Performed

There are three main methods of measuring eye pressure.

The most accurate method measures the force needed to flatten an area of the cornea.

* The surface of the eye is numbed with eye drops. A fine strip of paper stained with orange dye is held to the side of the eye. The dye stains the front of the eye to help with the exam. Sometimes the dye is in the numbing drops.

* You will rest your chin and forehead on the support of a slit lamp so that your head is steady. You will be asked to keep your eyes open and to look straight ahead. The lamp is moved forward until the tip of the tonometer just touches the cornea.

* Blue light is used so that the orange dye will glow green. The health care provider looks through the eyepiece on the slit-lamp and adjusts a dial on the machine to give the pressure reading.

* There is no discomfort with the test.

A second method uses a handheld device shaped like a pen. You are given numbing eye drops to prevent any discomfort. The device touches the surface of the cornea and instantly records eye pressure.

The last method is the noncontact method (air puff). In this method, your chin rests on a device similar to a slit lamp.

* You stare straight into the examining device. When you are at the correct distance from the device, a tiny beam of light reflects off of your cornea onto a detector.
* When the test is performed, a puff of air will slightly flatten the cornea; how much it flattens depends on the eye pressure.
* This causes the tiny beam of light to move to a different spot on the detector. The instrument calculates eye pressure by looking at how far the beam of light moved.

How to Prepare for the Test

Remove contact lenses before the exam. The dye can permanently stain contact lenses.

Tell your provider if you have a history of corneal ulcers or eye infections, or a history of glaucoma in your family. Always tell your provider what medicines you are taking.

How the Test will Feel

If numbing eye drops were used, you should not have any pain. In the noncontact method, you may feel mild pressure on your eye for a brief moment from the air puff.

Why the Test is Performed

Tonometry is a test to measure the pressure inside your eyes. The test is used to screen for glaucoma and to measure how well glaucoma treatment is working.

People over age 40 years, particularly African Americans, have the highest risk for developing glaucoma. Regular eye exams can help detect glaucoma early. If it is detected early, glaucoma can be treated before too much damage is done.

The test may also be done before and after eye surgery.

Normal Results

A normal result means your eye pressure is within the normal range. The normal eye pressure range is 10 to 21 mm Hg.

The thickness of your cornea can affect measurements. Normal eyes with thick corneas have higher readings, and normal eyes with thin corneas have lower readings. A thin cornea with a high reading may be very abnormal (the actual eye pressure will be higher than shown on the tonometer).

A corneal thickness measurement (pachymetry) is needed to get a correct pressure measurement.

Talk to your provider about the meaning of your specific test results.

What Abnormal Results Mean

Abnormal results may be due to:

* Glaucoma
* Hyphema (blood in the front chamber of the eye)
* Inflammation in the eye
* Injury to the eye or head
* Recent eye surgery

Risks

If the applanation method is used, there is a small chance the cornea may be scratched (corneal abrasion). The scratch will normally heal within a few days.

Alternative Names

Intraocular pressure (IOP) measurement; Glaucoma test; Goldmann applanation tonometry (GAT).

Additional Information

Tonometry refers to diagnostic tests that measure your intraocular pressure (IOP), or the pressure inside your eye. There are multiple methods available, and some don’t touch your eye at all. The various test methods can help your eye care specialist detect glaucoma before it causes permanent damage and vision loss.

Overview:

What is tonometry?

Tonometry refers to a type of eye test that measures pressure inside your eye (intraocular pressure). It’s one of the essential glaucoma tests. There are a few different methods and ways to do this test, all of which are quick and painless.

When is tonometry used?

Eye care specialists, especially ophthalmologists and optometrists, use tonometry to screen for and diagnose glaucoma. It’s a common part of routine eye exams and more specific exams when you have possible eye injuries or experience certain eye symptoms.

Eye specialists may also use tonometry to monitor your eye pressure if you’re taking certain medications. Monitoring your eye pressure makes sure that those medications don’t cause high intraocular pressure (ocular hypertension) as a side effect.

If you have glaucoma, regular tonometry determines treatment. Tracking your eye pressure is a key way to make sure treatment is effective, so frequent tonometry tests — including with devices you can use at home to take readings on yourself — are common.

Test Details:

How does tonometry work?

Tonometry measures the pressure of your eye’s anterior chamber. The anterior chamber is a fluid-filled space just behind your cornea at the front of your eye. Pressure from the aqueous humor fluid inside that chamber helps your eyes hold their globe-like shape. The unit of measurement for this is millimeters of mercury (mmHg), the same unit used for blood pressure tests.

Your eye care specialist can use a few different tonometry methods. Those include:

* Applanation tonometry. “Applanation” means “flattening,” and devices that use it have a small, disk-shaped extension that rests against your eye surface. The devices measure how much pressure it takes to make your eye surface start to flatten. This method is the most accurate. It’s common for eye specialists to use this method after other methods return unusual or concerning readings.
* Continuous monitoring. This method uses a sensor you wear on your eye like a contact lens. Researchers are investigating the wearable sensor and another, similar method that uses a surgically implanted sensor.
* Dynamic contour tonometry. These devices use a small, sensor-tipped extension that touches your eye (but doesn’t make an indention).
* Electronic indentation tonometry. Devices that use this method have a small probe that takes a measurement when it presses against the surface of your eye enough to make a small indention.
* Non-contact tonometry. Devices using this method push air at your cornea. The device then measures tiny, split-second changes in the shape of your cornea as the air bounces off its surface. Air puff tonometers do this with a small puff of air, while ocular response analyzers use a stream of air.
* Rebound tonometry. Devices using this method have a tiny, plastic ball that moves toward your eye and stops when it touches the surface. The device determines your intraocular pressure when the ball makes gentle, painless contact. Some devices that use this method are ones your eye specialist can prescribe for you to take and use at home.

How should I prepare for a tonometry test?

You shouldn’t need to prepare for a tonometry test. One exception is to make sure you don’t wear a tight collar doing the test (either by wearing another shirt or loosening the collar if possible). Pressure around your neck from your clothes can increase your intraocular pressure readings.

What should I expect during a tonometry test?

What you can expect from tonometry tests can vary depending on the method. If you’re having applanation tonometry, your provider will add eye drops containing an anesthetic and a dye called fluorescein to your eyes. But non-contact tonometry and most other methods don’t need either of these to work.

Some of the most common methods for the tonometry test only take a few seconds. Many of these faster methods work best with calculating an average of multiple readings, so don’t be surprised or think you’ve done something wrong if your eye specialist wants to retake the readings a few times. Other methods (like applanation tonometry) take up to a few minutes. Your eye specialist will tell you more about what to expect during the test.

What should I expect after the test?

Your provider can tell you the reading right after they take it.

If you received anesthetic eye drops, don’t let anything touch your eyes until the anesthetic wears off. Anesthetic drops keep you from feeling pain, so it’s easier to injure your eyes while they’re numb.

Is tonometry painful?

Tonometry shouldn’t hurt, even if the method used involves touching your eyeball in some way. If you have pain during the test, tell your eye care specialist. You can also ask them more about what to expect regarding that pain, including how long it should last and what you can do about it.

Results and Follow-Up:

What is a normal tonometry range?

A normal reading for most people is 10 mmHg to 21 mmHg. If your results are outside the normal range, there are a few likely next steps.

If your results are too high

If simpler tests show high pressure, your eye specialist will probably recommend using applanation tonometry to verify the readings. If applanation tonometry confirms that your pressure is high, your provider may monitor closely or offer treatment options. They’ll want to schedule regular follow-up visits.

Your eye specialist may recommend that you test your eye pressure at home. Be sure to ask about what to do if you get readings that are outside the normal range. You may need a follow-up visit with your specialist if you get slightly higher-than-normal pressures. But, if you get much higher readings, you may need emergency medical care.

Eye pressure that’s high because of angle-closure glaucoma is a medical emergency that needs immediate treatment. Without quick treatment, angle-closure glaucoma can quickly cause eye damage and permanent vision loss.

Other next steps can vary depending on your specific situation and needs. Your eye specialist can tell you more about what you can expect for your specific case.

If your results are too low

Low intraocular pressure is also a cause for concern since it can lead to eye damage and vision loss. Low intraocular pressure is usually anything under 5 mmHg or 6 mmHg. If the pressure in your eye is too low, your eye specialist will talk to you about treatment options and follow-up visits to monitor your eye health.

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