Heart Surgery 101

In 2005, I was asked to write a piece for KnowledgeNews.net. This piece is copied below, with a few minor additions. It was prompted by the fact that former President Bill Clinton was undergoing a second open heart procedure. The piece was titled Bill Clinton’s Heart* and began like this:

“Today former President Bill Clinton will reenter the operating room, and surgeons will reenter his chest-fixing problems created when they did coronary bypass surgery last year. Surgeons are never happy about revisiting previous work sites. Once violated, your body’s tissues heal with scarring, and scar tissue obliterates the nice, neat, anatomical planes that make most surgical operations predictable.”

It’s purpose was to answer this question:

“How will President Clinton’s doctors do their delicate work? How does heart surgery really work?” Here is how, and even 17 years later the setting and procedures are pretty much the same, though the technology and materials have all continued to improve.

Setting the stage

The patient lies in the middle of the cardiac surgical suite, flat on his back under bright lights, painted with an ochre iodine solution from neck to knees, then draped in multiple layers of sterile plastic and cotton. A vertical screen separates his head and neck from the site of the surgical action.

Behind this screen, the anesthesiologist does his magic, infusing a cocktail of oblivion­ inducing drugs into the patient’s veins, inserting a tube down the windpipe, and ventilating him with a mixture of gases that keep consciousness mercifully at bay. On the patient’s left side, the pump team sets up shop, with a technician seated behind a low, rectangular stainless steel machine the size of a large desk. He’s all about plumbing, preparing the tubes that, within the hour, will carry blood from the patient’s stilled heart to the machine, through a cylinder where the dark purple blood picks up oxygen and turns cherry red, and then back again to the patient’s aorta for distribution to the body. Raised over the end of the table is a mammoth tray of tools–surgical hardware.

Getting in

The surgeon and scrub nurse wait on the patient’s right, the surgical assistant on the left. With one vertical slice down the middle of the chest and a buzz of the saw down the center of the breastbone, or sternum, the chest wall is breached.

The surgeon wedges a nifty little tool into the sternal split, and proceeds to crank open the chest. (At the end of the surgery, he will use something that looks like a meat hook to wind up the wire sutures that pull the edges of the bone back together. And later write a prescription for enough narcotics for several weeks.) As the bone comes apart, a shiny pink pillow puffs up from below, filling the gap. This is the lung, protected in a slippery, clear envelope called the pleura, which lines the inside of the chest wall and the outside of each lung, letting the lung slide friction-free as it expands and contracts.

With the bony gap widened to six or seven inches, the surgeon removes the spreader and gently pushes aside the right and left lungs, covering them in wet, protective cloths. He is now in the middle compartment of the chest, the mediastinum. There, in the center, in a protective, transparent little envelope called the pericardium, is the heart–a purplish, muscular little fist of an organ in its healthy state, pumping away with a powerful twisting contraction. Of course, since we’re doing heart surgery for a reason, it might be a pale, flabby bag, draped in yellow fat, contracting with a weak little squeeze.

Getting the Job Done

Getting in is the standard part. What happens next depends on what the patient needs. Sometimes it’s a new valve inside the heart, or maybe two. Sometimes it’s bypassing diseased coronary arteries on the surface of the heart with an artery brought down from the chest wall and attached beyond the blockage, or with a piece of a vein from the patient’s leg attached at one end to the aorta and at the other end beyond the blockage. Either way, the stitch work is so tiny that the surgeon wears glasses with little microscopes on the lenses.

Sometimes a bypass can be done without stopping the heart, and the surgeon sews in rhythm with the beat. But most times, the surgeon has to re-plumb the body, sending un-oxygenated blood from the right side of the heart out to the mechanical pump and depending on the pump technician to run the machine and send the blood back to the aorta. Then the surgeon stops the heart with a mixture of drugs, letting it lie peacefully in the center of the chest while the repairs get done.

Getting Out

Going on the pump and coming off the pump can be white-knuckle times. Sometimes there is trouble restarting the heart. Sometimes the patient has to go back on the pump. But if all goes well, backing out is largely the reverse of getting in, with many checks in place. All the tools and all the gauze sponges used for mopping up must be back where they belong (it’s surprisingly easy to lose things in a blood-soaked operating field). The inside of the chest has to be dry (no leaking of blood from anywhere). Even then, tubes are left in place in the chest to let oozing fluids drain to the outside for the first few days of healing. These come out several days later, with a hard yank and a stitch or two to close the hole. Then the sternum gets pulled back together with wire – it stays in there permanently. If the surgeon likes music in the operating room, and all has gone smoothly, the music sometimes gets changed to something a little livelier, and the skin gets sewn up. The surgeon’s work, he hopes, is done. It’s nature’s time to go to work and smooth over all the cuts and stitches.

*KnowledgeNews, Thursday, March 10, 2005

Anxiety: A Protective Emotion

“…Kids are different today, ” I hear every mother say
Mother needs something today to calm her down
And though she’s not really ill, there’s a little yellow pill
She goes running for the shelter of her mother’s little helper
And it helps her on her way, gets her through her busy day…”

                                  Mother’s Little Helper, The Rolling Stones

    In 1966, a bluesy rock song penned by Keith Richards of The Rolling Stones paid homage to the tranquilizing drugs which had become the rage, in an age of anxiety defined by the “rat race” and by the development of the psychopharmacologic approach to life’s problems. The title of the song, Mother’s Little Helper, reflects the predominance of women as the recipients of drugs that treated anxiety and the lyrics are a succinct representation of the dilemma of the diagnosis of anxiety. Is anxiety a mental illness, and, if not, what is it?

    Anxiety has been defined in many ways over thousands of years. For the classicists of Rome and Greece, the words used to describe anxiety as illness were nuanced.  Some referred to a mental feeling and others to bodily sensations, and they all conveyed a sense of constriction. As far back as the oldest book in the Bible, the character Job, in his anguish, speaks of “the narrowness of my spirit.” A different aspect of anxiety appears in one of the Romance languages, in the Romanian word nelinişte, meaning unrest. Between the ancients and the modern era of psychiatry, the concept of anxiety as a unique disorder goes dormant, with the symptoms buried in other diagnoses referring to emotions, particularly melancholia and neurasthenia. But by the time of the first Diagnostic and Statistical Manual of Mental Disorders in the early 1950s, anxiety was back, categorized as a mental disorder, with progressively more sub-categorizations related to associated behaviors over the next four updates to the guide. Anxiety disorders are said to affect almost a third of US adults at some point in their lives, and are rising among children as well.

    There are clearly people for whom the emotion of anxiety is crippling, interfering with the ability to navigate in the world, to accomplish necessary tasks of daily life, and to use the potential they have to live the best life they can. For these people, anxiety is a disorder. And anxiety complicates other serious mental illnesses like depression and schizophrenia. But anxiety is also normal, a feeling of dark expectation that is part of being human. Everyone experiences anxiety intermittently. Sometimes it keeps us awake. Sometimes it interferes with plans. Sometimes it helps us avoid problems. Sometimes it lingers longer than usual. Given the very high frequency of anxious feelings, learning about why anxiety occurs and about how to cope when it appears may be very helpful.

Anxious feelings are a protective. Because we are vulnerable creatures in a world filled with danger, we evolved to recognize, respond to and figure out how to avoid things which threaten us. The parts of the brain charged with this task are the amygdalae, paired almond-shaped structures deep in the brain on each side, near the temporal lobe. The connections to and from the amygdalae are complex and extensive, and the circuits trigger two emotions when we face unfamiliar, potentially threatening situations: fear and hope. Fear focuses attention and freezes motion, while triggering the physiologic responses necessary to fight or flee. Hope is the emotion that emerges when memory scanning triggered by the amygdalae yields recognition of a pattern in the threat. Hope enables development of a plan of action. Anxiety is the dark apprehension we feel when we cannot find the way to a plan to deal with persistence of the fearful, or just plain unresolved situation.

   Anxiety has three components. First, an alarm reaches each amygdala through the senses and triggers fear and memory scanning. The alarm encounters the second component, a mixture of beliefs based on prior experiences stored in memory.  The third component is the coping behavior that emerges.  Coping behaviors may be unsuccessful in reducing the fear, or unable to resolve the situation because of conflicts with beliefs.  When coping is unsuccessful at restoring calm, anxiety carries on, a dread sense sometimes accompanied by restlessness, nervousness, tension, sweating, weakness, shaking, rapid heart rate and hyperventilation, spilling over into non-threatening situations. When normal life is compromised, or unsuccessful coping behaviors like substance abuse take over, anxiety becomes a mental disorder.

    Some of us have more anxious temperaments than others, but everyone can work to better cope with fear-provoking situations. The less chaotic our lives, the fewer the confrontations with the unknown are – but control can never be perfect and lack of control itself can cause fear and, hence, anxiety. many of the patterns we establish in our lives, such as regular habits and ordering our environments we have learned unconsciously as a means of keeping anxiety under control. Countermeasures like the techniques of cognitive behavioral therapy (CBT) are not only useful but can be done as self-help. There are numerous cognitive behavioral therapy resources available in libraries and online. They teach recognition of the common distortions of thinking that lie beneath chronic anxiety, and ways to correct them. Interestingly, CBT is quite similar to the recommendations of the classic Epicurean and Stoic philosophers who wrote about anxiety so long ago.

    When anxiety disrupts life and does not yield to attempts to change, the professional help of a cognitive behavioral therapist is in order, as well as a general medical checkup to rule out problems like hyperthyroidism or Vitamin B12 deficiency.  Sometimes a therapist will add a pharmaceutical product, usually one in the SSRI category of antidepressants. While the “mother’s little helper” class of drugs, the benzodiazepines, are very effective in reducing acute anxiety, more chronic use has led to significant, refractory addiction problems, and SSRI-type antidepressants are a better choice to begin with if drugs are going to be tried. If drugs are employed they should not be a substitute for the hard work of understanding how the interaction of personality, experience and environment lets a useful and protective emotion become untethered from its purpose. Such understanding can help the mind move forward into solutions.

Two Years In

Below I have copied a comment I wrote in January 2022 on an article published on Substack by a biologist who named Joomi Kim. Joomi’s website is linked below. The article, titled “I Was Deceived,” is robustly documented and I had begun sending a link to it to friends who wanted more information about the 2019 pandemic virus and the medical approaches to it. I wrote the comment because I have spent many hours a week for the last two years delving deep into the science behind the pandemic narrative, keeping family and friends who wanted to be informed up to date, and I was grateful have the compilation of references that were attached to Joomi’s story. The comment, in addition to being a thank you note to Joomi, is a brief description of my own conclusions about what has happened and where we stand now.

During the spring of 2020 I realized that something was very wrong in the medical world of COVID – terrible data collection and a peculiar indifference to attempting to treat patients with the infection until they were late in the illness, when they were essentially untreatable. In the summer of 2020, I sat down with my iPad, in a small town in the mountains, to investigate the PCR test which seemed to be the linchpin of the “pandemic,” the thing that defined the numbers that were being used to justify destruction of social bonds and economic activity. I got up two hours later, realizing that surely the people behind the lockdowns and the health care directives knew what I now knew, and I sadly came to the conclusion that the exercise we were enduring was not about our welfare, but about getting to the great vaccination project. I’ve learned more about virology and immunology and the psychology of crowds than I ever wanted to know, and have found all that you have written here – and more. I am afraid that the myocarditis and aggressive cancers are just the tip of a very large iceberg and I believe we are involved in the greatest public health disaster in history. I am very grateful to you for having compiled all of these links in one place and intend to give this article to anyone I come across who is beginning to wake up to what has happened.

You can find the January 15, 2022* article on Joomi’s Substack site, found at:    https://joomi.substack.com/

*The title on the author’s main page is “I Was Deceived.”I have deliberately linked to the author’s main page rather than to the article directly because its URL title is one that could be flagged by the WordPress administrators as disinformation. This is the world we live in now.

Cytokines and Inflammation: Balance Required

Inflammation is bad, right? Chronic inflammation has been implicated in cardiovascular disease, type 2 diabetes, non-alcoholic fatty liver disease, cancer, autoimmune diseases, Alzheimer’s disease, other neurodegenerative disorders and more. Ad campaigns for new anti-inflammatory drugs are everywhere, and the best-selling over the counter pain relievers, taken by millions of people, work by suppressing inflammation. It is easy to get the impression that inflammation is always detrimental to health. But, without inflammation, all injuries would be permanent and our defenses against bacterial and viral invaders would be feeble. The inflammatory process is vital to life, the necessary first step in healing and in the body’s defense against infection.  But there is a dark side to this finely tuned system.  Inflammation can become chronic, outlasting the need for defense and repair, and damaging normal tissues in the process.

How inflammation works

Inflammation begins the when cells send out signals that they have been injured, by thermal or physical forces, or attacked, by organisms like bacteria or viruses. The language of this cellular communication is chemical, involving messenger molecules called cytokines (cyto meaning cell and kine, from kinos, meaning movement).  Cytokines attract of white blood cells to the area of injury, and they open pores in nearby tiny blood vessels to let in this defensive army, along with variety of specialized proteins that begin the job of healing.  Inflammation is the word used for the changes that occur in tissues as a result of the orderly events that ensue. With successful healing, signs of inflammation subside, and cellular cytokine production returns to the baseline level necessary for routine cellular maintenance and regeneration.

The normal course of healing inflammation

The cardinal signs of inflammation are redness, heat, swelling and pain. Redness, heat and swelling come from the increase in blood flow and permeability of the blood vessels. Pain is the result of cytokine stimulation of tiny nerve endings, and serves the purpose of limiting movement to limit further damage.  Some cytokine signals reach the temperature control centers in the brain, raising the body temperature to levels invading organisms tolerate poorly. Specialized immune cells immobilize and kill viruses and bacteria and cleanup cells called macrophages clear the debris. Gradually, dead and dying cells are walled off and disposed of. Rebuilding begins, taking advantage of scaffolding produced by the proteins which have leaked from the blood and caused clots to from. You see this process every time scab forms on a cut and later shrinks and peels away to reveal new skin cells beneath.

Maladaptive inflammation

But sometimes the inflammatory system does not gear back down, resulting in tissue damage rather than repair. This control failure may be rapid and catastrophic, the so-called cytokine storm, a term which has become familiar during the 2020 SARS-COV19 pandemic. It describes the damaging effects of an overreaction of the inflammatory response triggered by the immune system during infection or severe trauma. Oncoming cytokine storm cannot be predicted based on routine clinical parameters or tests, but researchers are beginning to tease out more sophisticated chemical markers of inflammation which correlate with more severe disease.

Maladaptive inflammation can also be slow and chronic, with progressive tissue damage like that which occurs in rheumatoid arthritis. The causes of such chronic inflammatory responses are legion and many don’t have obvious relationships to the normal inflammatory pathways. They include obesity, inactivity, toxic chemicals in food and the environment (xenobiotics), poor sleep, chronic infections and antibiotics that alter the normal bowel bacterial populations. Chronic inflammation is also a result of autoimmune responses to the body’s own tissues – cross reactions between immune responses to external agents and to the body’s cells, particularly in skin or joints and other organs like the thyroid gland. No one understands exactly why these self attacks begin to occur but autoimmunity is on the rise in all age groups.

Intertwined systems

The wide ranging influences on the inflammatory system reveals the deep connections between the body’s different physiologic systems. Disruption in one system influences production of chemical signalers in another. For instance, stress and lack of sleep suppress normal defenses against infections. External factors as simple as poor mechanical care of teeth allow chronic gum infections to take hold. Smoking and air pollution irritate the lungs. Lack of exercise changes the way blood flows though arteries, setting them up for damage and chronic inflammatory repair processes. And chronic use of anti-inflammatory drugs for aches and pains alters the finely tuned balance of cytokine signaling throughout the body. 

As we age, chronic inflammatory markers – measurements of some select cytokines like C-reactive protein – tend to rise. Attention to diet, exercise, sleep, dental care and stress management are within your control and help suppress inflammatory marker levels. Removal of allergens and irritating chemical triggers like smoke from the environment helps, as does attention to areas of the body that are sites of chronic infection, like teeth and skin.  

Pharmaceutical interventions are common ways of suppressing chronic inflammation. The NSAIDS, non-steroidal anti-inflammatory drugs like Advil, block cytokines called prostaglandins. Most recently, drugs-called biologicals target individual cytokines by blocking them with antibodies. The new biological drugs provide significant relief to people who suffer from autoimmune problems, but they can also impair the primary functions of defense and repair. Caution is required and risk-benefit calculations are necessary, because opportunistic infections – ones that the body normally handles well – can take hold and thrive. The body’s innate cancer surveillance system, which finds abnormal cells and induces their death before they become malignant, can also become less functional.  

Maintaining the Balance 

Cytokines and the inflammation they cause are part of an enormously complex, finely balanced cellular maintenance and body defense system. Small disruptions in the balance over time, such as happens with chronic use of anti-inflammatory drugs for treatment of pain, or chronic stimulation from infection, can show up in odd and seemingly unrelated ways, like an increased rate of heart attacks and strokes in chronic NSAID users and development of liver cancer in hepatitis sufferers. In an imperfect world, perfect balance is hard to maintain, but the inflammatory response system is far more often good than bad.    

Blood Clotting…and Not Clotting

    Over a gallon of blood circles your body every 45 seconds, under pressure, in a network of arteries, veins and capillaries.  Any leaks in the system must be plugged and repaired. Some ruptures are emergencies requiring outside help, but most are fixed handily by a well calibrated system of physical and chemical reactions in your body.  You watch this process every time you cut yourself shaving or slicing tomatoes, but it also happens microscopically, all over your body, when blood vessels are damaged internally by trauma or infection or chronic degenerative changes in the walls of arteries.  

How clotting happens 

Hemostasis, the first step in controlling bleeding, involves mechanical measures like pressure, cautery or stitches to stop blood flow from damaged blood vessels. Hemostasis alone is ineffective and must to be accompanied by blood clotting, a process triggered by blood platelets, which are tiny little disc shaped cell fragments that accumulate at the site of blood vessel injury. About a trillion platelets circulate in the blood, speeding by over 10,000 square feet endothelial cells that line the inside walls of blood vessels. When damage exposes collagen and other proteins in the endothelial cells and surrounding tissues, platelets gather to plug the defect, while secreting chemicals that draw white blood cells to the scene. An orderly sequence of chemical reactions, known as the clotting cascade, then produces in a stringy mass of sticky protein called fibrin, which fills the gaps between the platelets. Over the next few days to weeks, as healing proceeds, the clot gradually dissolves and disappears in a process called lysis. Your scab falls off to reveal new skin underneath.

Balance between clotting and not clotting

Blood also must not clot to carry out its normal function of transporting oxygen and carbon dioxide and nutrients and waste. If blood clots occur inside blood vessels, they block blood flow and cause damage in surrounding tissues. Health problems like strokes and heart attacks, and clots in the heart, lungs and leg veins occur because local conditions like inflammation and slow blood flow trigger the clotting process. For example, when atrial fibrillation causes failure of atrial pumping, blood pools in the recesses of the upper chambers of the heart and clots may form.  Slow and turbulent blood flow in arteries narrowed by inflamed cholesterol plaques sets off the clotting process. Immobilization, bed rest or even prolonged sitting can promote clot formation in the leg veins.

Manipulation of the clotting system

Health problems like these, as well as the need to hasten clotting in some medical situations, drive attempts to manipulate the clotting system. Infusions of platelets and other blood products correct bleeding in the operating room and in medical conditions that lead to poor clotting, but, more commonly, medical problems require suppressing the blood clotting response. Most people are familiar with anti-clotting drugs, called “anticoagulants,” that interfere with one or more of the chemical processes in the clotting cascade. They are used for common heart problems like atrial fibrillation, leg vein clots and after heart valve replacements to prevent the foreign valve materials from triggering clotting. Most people are also familiar with “antiplatelet” drugs like aspirin used to help prevent heart attacks and strokes by interfering with the ability of platelets to start the clotting process. 

Pharmacological aid in breaking down clots 

A third type of intervention employing “thrombolytic” drugs aims to dissolve clots that have already formed.Thrombolytic drugs are used in hospitals, in the acute setting of clots that have caused heart attacks and strokes. When injected into arteries, they dissolve clot and restore blood flow though the problem area of the blood vessel that triggered the clotting process, or through an artery in the brain that has been suddenly blocked by a clot that traveled there from the heart.

Blood “thinners”

 Anticoagulant drugs are often incorrectly called blood thinners, but they do not change the thickness of blood. They block reactions in the clotting cascade. Heparin, when injected intravenously, causes the most direct and immediate interference, so doctors opt for this choice (or other similar drugs if a patient is allergic to heparin) when stopping clot formation is urgent. The insertion of an artificial heart valve, which will trigger clot formation on its surface, the presence of leg clots which may break off and travel to the lungs, or the onset of atrial fibrillation call for prompt blocking of clot formation, while the transition is made to oral anticoagulant drugs.

Oral anticoagulant drugs take a few days to slow the speed of blood clotting.  Of the oral drugs available for blocking clotting, coumadin is the oldest and most frequently used because its anticoagulant effects can be stopped quickly, if necessary. The ability to reverse anti-clotting effects is important if the anticoagulated patient develops a bleeding problem or is at risk of falling or other injury. Coumadin’s effects are reversed by intravenous injection of Vitamin K. People taking coumadin must have their blood checked regularly to monitor the rate at which the blood clots, and adjust doses accordingly. Other newer oral anticoagulants are popular because they do not require testing, but are more expensive and their effects cannot be reversed as quickly.  Intramuscular drugs are available for home use, usually when anticoagulation is a temporary treatment.

Drugs that make platelets less sticky

Antiplatelet drugs like aspirin and persantin are often prescribed to prevent clot formation in the coronary arteries, though the evidence about their benefits is mixed.  Far more common, however, is the unsuspected antiplatelet effect encountered by people using many over the counter products, particularly non-steroidal anti-inflammatory drugs (NSAIDS) used for pain, and some supplements like fish oil. Aspirin and NSAIDS are implicated in stomach bleeding episodes and in heavy menstrual bleeding.

 In addition to its role in repairing leaks and keeping blood running freely through the vast network of blood vessels in the body, the complex chemistry of the blood clotting system is revealing itself to be intricately involved in other aspects healing and in immune-mediated inflammatory states (such as COVID-19). The attempt to immunize against the SARS-COV2 virus has also focused attention on blood clotting, with the antigen chosen to stimulate antibody formation triggering serious adverse events involving both clotting and bleeding, as well as unsuspected clot formation in very small blood vessels. Knowledge is accumulating rapidly and, as it does, expect to see blood platelets revealed as much more than pieces of cells used to plug holes and the clotting system more closely related to the inflammatory system.  

Trigeminal Neuralgia: The Worst Head Pain

Anyone who has experienced toothaches, blocked sinuses, earaches, corneal scratches or migraine headaches knows that pain arising from any part of the head can be severe. Head pain is transmitted to the brain through the fifth of twelve pairs of cranial nerves at the base of the brain, named the trigeminal nerves. The worst head pain of all is the result of one or the other of these nerves misfiring, a condition known as trigeminal neuralgia, in which hundreds of episodes a day of lightning like spasms of pain on one side of the face are triggered by trivial touch or movement or by nothing identifiable. The pain is severe enough to bring sufferers to their knees and to cause more than a few to say that if it persisted they would have to commit suicide.  The famous painting, The Scream, by Norwegian artist Edvard Munch, has been called a visual representation of the agony caused by trigeminal neuralgia.


Symptoms of trigeminal neuralgia are almost always one-sided.  Spasms of facial pain are brief and explosive and described as stabbing, electrical, or like being stuck with an ice pick. Episodes can last for weeks or months, and then disappear not to return, or they may return in similar fashion, without warning, months or years later. Pain bouts may also become chronic and associated with other duller, longer lasting pain in the same area of the face. Because light touch and facial movements such as chewing and talking can trigger pain, patients avoid eating, lose weight, become depressed and socially withdrawn and look disheveled from avoiding skin care and shaving.   

Why does it happen?

About 150,000 new cases of trigeminal neuralgia are diagnosed in the US every year, more often in women than men and usually over age 60. The ailment can appear in younger people, most often in conjunction with multiple sclerosis. As long ago as the eleventh century, an Arab physician, Jujani, suggested that a blood vessel in the head, near the nerve that served the face, caused spasmodic facial pain and anxiety, a prescient notion since one of the few risk factors for trigeminal neuralgia is high blood pressure. Chronic high blood pressure distorts and hardens arteries, and one of the most effective treatments of trigeminal neuralgia in modern times has been to pad the nerve, protecting it from the pounding of an overlying artery.

Bolstering Jujani’s theory, pathological examinations of trigeminal nerves have shown evidence of damage and repair to the sheaths surrounding individual nerve fibers, suggesting that pressure from a nearby artery or vein, causes intermittent, reversible damage. The association of trigeminal neuralgia with multiple sclerosis, an inflammatory disease which also causes myelin sheath damage, lends weight to the idea that stripping sensory nerve fibers of their myelin sheaths somehow causes them to be irritable and misfire. There is no specific test for trigeminal neuralgia, which can be diagnosed from the clinical history alone. However, sometimes CT and MRI scans are done to rule out tumors irritating the trigeminal nerve, or to look for evidence of demyelinating diseases like multiple sclerosis or other autoimmune problems. Spinal fluid analysis might be added a search for inflammatory or demyelinating marker proteins and cells.

Similar conditions

      Other conditions may produce shooting head pains. One is glossopharyngeal neuralgia, coming from irritation of a different cranial nerve and causing pain deep in the throat and ear. It is much rarer than trigeminal neuralgia, but medical treatments are similar. Another is occipital neuralgia which comes from compression of a nerve in the upper neck, at the base of the skull. This painful condition is associated with poor posture, trauma or arthritic changes. Occipital neuralgia presents itself as stabbing or shooting pains, as well as duller aching pain and general headaches in the back and sides of the head, and at times behind the eyes. Temporomandibular joint problems (the joint that hinges the jaw to the skull) may also cause shooting pain in the side of the face, along with jaw pain and locking.


    The first effective treatment of trigeminal neuralgia was based on the concept of nerve cell irritability, with the use of drugs that treated seizures, first introduced in the mid-1900s. Though not perfect, these drugs continue to provide significant relief for the majority of trigeminal neuralgia sufferers. In addition, many attempts have been made to change the input of the trigeminal nerve to the brain physically by cutting it or injecting it with chemicals that deaden it. This treatment is called neuro-ablative surgery and the relief obtained is in direct proportion to the amount of numbness in the face caused by deliberately damaging the nerve. The more numbness, the better the pain relief. However, for some people, persistent facial numbness or unpleasant sensations are almost as intolerable as the pain, so numerous variations on such procedures have been tried. There are few controlled studies of outcome. Gamma knife surgery is the latest method. Symptoms recur within three years in 20-60% of patients, in inverse proportion to the amount of numbness produced by this deliberate nerve damage. 

    Microvascular decompression surgery (MVD), as mentioned above, is the most effective surgical procedure for trigeminal neuralgia. It involves opening the skull and placing a Teflon felt pad between the trigeminal nerve and the blood vessel that lies atop it, just where the nerve enters the brain stem. In experienced hands MVD produces immediate pain relief in over 90% of cases, with relief sustained for a decade or more in over 2/3 of them. Though many patients would rather try this or other surgical procedures than be dependent on anticonvulsant drugs, they must carefully weigh the risks, which are those of general anesthesia and of opening the cranial cavity, infection and damage to delicate neural structures chief among the possibilities. Procedures such as these should be done in centers where experience levels of all involved are demonstrable.

     All the pains we suffer are reminders that our exquisitely complicated pain networks exist to guard the body, particularly the head and the brain within, against damage from the environment. Like every other part of the body, the pain systems can go awry, making life very difficult, but this is nature’s trade-off since life without pain is more dangerous. In conditions like trigeminal neuralgia we are left to try to understand the cause and to intervene as best we can without causing harm.

Mole or Melanoma?

    In ancient mythology, moles were dark spots sent by jealous gods to spoil the faces of beautiful people. Later, moles became signs that the soul had fled the body, a notion that shows up today in Halloween witch masks with hairy warts sprouting from noses. In the 1800s, imitation moles made of leather, velvet and mouse fur covered pox scars in the aristocracy and led to their rebranding as beauty marks. Modernity continued this tradition with some famous stars like Marilyn Monroe enhancing their moles cosmetically. However, modernity also gave rise to the fear of moles because of worry about the most serious form of skin cancer, the melanoma. Most people have moles somewhere on their body. How do you know which ones to worry about?

Melanocytes: the origin of dark spots

    Before you begin worrying, you need to know what you are worrying about. The problem with moles is that, though the vast majority are quite benign, they come from the same type of cells that give rise to the dreaded melanoma. These cells are called melanocytes, one of three types of skin cells.  They make the pigment melanin that gives skin its color and protects it against ultraviolet light, the kind that produces sunburn. Melanocytes store melanin in little capsules inside themselves, ramping up production when the skin is exposed to sunlight, and distributing it to the outer skin layer where cells called keratinocytes absorb it.  Moles, which are technically known as melanocytic nevi, are clumps of melanocytes which appear as dark, often raised spots anywhere on the skin. They are regular shaped with smooth edges, evenly colored, and generally less than a quarter of an inch in diameter. Moles are not freckles, which are discrete spots of reddish-brown keratinocytes that appear mainly in very fair-skinned people because the melanin distribution process in their skin is uneven.

Moles: the cloning of well behaved rogue cells

    Babies are rarely born with any moles. Melanocytic nevi begin to appear in childhood and continue for several decades, peaking in the thirties. Most people have between 10 and 40 moles by adulthood.  Sometimes they begin to reverse and disappear. Recent research suggests that a mole appears when a rogue melanocyte begins to clone itself. This sounds like the same process that begins cancer, and, indeed, initial melanocyte growth involves genetic changes similar to those seen in cancer cells. But in the case of the mole, there appear to be controlling processes at work that prevent continued growth and organize the cells into well-defined architecture characteristic of non-cancerous growths. But will it turn into a melanoma – a cancer which may spread both locally and distantly?

Melanomas: Rogues without controls

    Most moles are and remain benign throughout life. Melanomas, though, are increasing in frequency in recent decades. Projected numbers of new melanoma diagnoses in the US in 2019 estimate over 96,000 cases, more in men than in women.  Deaths from melanoma will exceed 7,200.  Melanomas are twenty times more common in white skinned people than in dark skinned. About 25-30% of these melanomas will arise in previously stable, benign moles, but it is not at all clear that the mole is the source. They may be just as random in their appearance there as they are in any other part of the body. Melanomas also begin with rogue melanocytes, but they lack the control mechanisms of the offspring of the melanocyte that gives rise to a mole. They are biologically different from the cells in moles.

Markers for melanoma risk

    What increases the risk for melanoma development? Fair skin and freckling, a family history of melanoma, chronic unprotected sun exposure, large numbers of nevi, and biopsies showing irregular (dysplastic) features under a microscope. Large number of moles – in the range of 100, also increase the risk that a melanoma will appear in a previously benign spot.  Some melanomas appear in unexposed areas of the body, inside the mouth and in the eye, suggesting that they are different biologically from melanomas that occur in sun-damaged skin.  

Early recognition helps

    Early recognition of a melanoma improves the outcome. Five-year survival rates when the tumor is localized in the skin is 98%. With spread to regional lymph nodes, survival falls to 68% and down to 23% with spread to distant lymph nodes and other organs. Overall five-year survival is 92% and improving with the advent of newer forms of treatment based on immune attack of the tumors.

    Early recognition of melanoma depends on two things – knowing your own moles and examining them and the rest of your skin for any changes on a regular basis. Self-examination means using a mirror or asking a partner to help with scrutiny of your head and backside. What are you looking for?

  1. New spots with irregular color or borders. But every new spot, especially in older people, is not cause for worry. Many are so called age spots – flat, brown, over-pigmented areas. Others are overgrowths of keratinocytes called senile or seborrheic keratoses.
  2.  Change in old moles, especially irregularities in color or shape. Some melanomas may be pale, not dark. Some may have multiple shades. Some are relatively smooth but others may be bumpy.
  3. Growth in size happens to moles at times, particularly with hormonal change, or with sun exposure, and growth alone is a poor predictor of whether or not a mole has transformed to a melanoma. Growth with change in color or border irregularity is more worrisome.
  4. A bleeding mole, or failure to heal if the surface is disturbed. 

A biopsy is the only way to know for certain that what a change in a mole, or a suspicious new spot represents, and regular examination by a dermatologist eases worry, especially if you have a family history of melanoma or an unusually large number of moles. And it is never too late to protect your skin from the sun, by avoiding exposure during the height of the day, by covering skin with clothing, and using sunscreen in unavoidably exposed areas.

Restless Legs

       In 1999, Dr. William Dement, the nation’s foremost sleep researcher, lamented that 15 to 20 million Americans with Restless Leg Syndrome had fallen into a major knowledge gap in the medical care system.  Doctors simply didn’t recognize the symptoms, and, more importantly, didn’t understand the serious effects of restless legs on patients’ lives.  Dr. Dement wanted to educate patients and their doctors, but sleep medicine didn’t attract much public attention.  Then, in 2006, the pharmaceutical industry waded into the knowledge gap, launching an advertising campaign during the Superbowl for the first drug approved for the treatment of Restless Leg Syndrome, something most of the audience had never heard of.  Advertising a disorder to market a drug is not the education Dr. Dement had in mind, but at least it generates interest and curiosity, the first steps toward knowledge.

      “Syndrome” means a set of symptoms. Restless Leg Syndrome (RLS) encompasses creepy, crawly sensations in the legs (but occasionally in the trunk muscles or arms), occurring mainly in the evening, getting worse on retiring for the night, and relieved by motion, particularly walking.  The best estimates are that 5-15% of the population recognizes these symptoms as their own. More men than women are affected and frequency increases with age. The cause is unknown, but recent research suggests that iron metabolism in a tiny part of the brainstem is at fault.  

       RLS is also known as “Ekbaum’s Syndrome,” after Karl Ekbaum, who first described the problem in 1940.  Jerry Seinfeld’s script writers added “Jimmy Legs” to the RLS lexicon when they had Kramer moan about a girlfriend whose nocturnal leg movements made him crazy. Kramer was actually describing not RLS but the primary sleep disorder that often accompanies it: periodic leg movement disorder (PLMD). In contrast to restless legs, Jimmy Legs often bother bedmates more than they do the afflicted sleeper, who spends much of the night bicycling away with no memory at all of the movements or of the multiple awakenings that accompany them.

More than a sleep disorder

     Because restless legs cause insomnia and sleep deprivation, RLS is technically a sleep disorder. However, the sufferer’s waking world is also fraught with difficult situations that demand stillness. Theaters, airplanes, dental chairs – even operating tables- can be intolerable. The course of action taken for relief depends on the frequency and severity of the symptoms, balanced against the risks and side effects of the treatments considered.

     The mildest version of RLS occurs in otherwise normal people after extreme physical exertion such as running a marathon, and it responds to time, rest and energy replenishment. At the severe end of the RLS spectrum are people whose trouble falling asleep and disrupted nighttime sleep produce severe daytime sleepiness. They need accurate diagnosis and treatment, by sleep specialists if possible.  Between the mild, intermittent end of the spectrum and the severe extreme are all the rest of the RLS sufferers, including some pregnant women. These people are best served by an ongoing relationship with a doctor who understands the syndrome and the complete approach to treatment.

Diagnosis and Treatment

       Treatment begins with a good history and physical exam. Restless legs are sometimes symptoms of peripheral nerve or kidney problems, and occur in the setting of diabetes. They can also reflect side effects of drugs such as antidepressants, antihistamines, and anti-nausea medicines. Even in the absence of medical problems, a check of the serum iron is on order since long clinical experience and new research implicate iron metabolism. Iron deficiency should prompt a search for a cause – usually bleeding or dietary insufficiency. Medications to reduce stomach acid, now in widespread use, can also cause iron deficiency.

         Assuming there are no underlying medical problems, the next step is the elimination of stimulants from the diet – particularly in the latter half of the day. That means caffeine, cigarettes and alcohol – as well as any over the counter medicines of the types mentioned above. Developing mental alerting strategies to occupy the mind during times of boredom may help. When focused and occupied with games or puzzles the brain seems to suppress restless impulses. Increasing daily physical activity quiets the legs in over 50% of RLS patients.

          When sleep suffers and normal life situations such as long automobile rides are intolerable, pharmacologic intervention is often necessary. The drugs that appear to be helpful fall into four classes: the ones that increase the neurotransmitter dopamine or act like dopamine (dopamine agonists); narcotics like codeine; the benzodiazepines like Valium, and the anticonvulsant Gabapentin. All of these are serious drugs with potential side-effects, not the least of which is a phenomenon called augmentation – the worsening of symptoms over time producing the need for more drugs.  But the drugs can be true life-savers for people who are severely afflicted and in desperate need of sustained sleep and the ability to remain still.

       What of the new drug touted in Superbowl ads in 2006, and a more contenders released since then? They are dopamine agonists, some of which  have been around for years – FDA-approved for use in Parkinson’s disease, but also used “off-label” by doctors dealing with RLS patients. Their marketing focuses a light on the obscure world of sleep medicine, where devoted researchers who followed Dr. Dement continue to educate patients and doctors about the troubled sleep that generates many accidents and eats away at productivity and emotional resilience. That is a service to all.

The Legacy of Smallpox: Immunization

Imagine a virus spreading disease in your city. Imagine sending your children and other loved ones to a rural area to be injected with infected material taken from people ill with the virus. Imagine the injections making them sick, but not as sick as they might be from contracting the disease naturally. They will require a month for recovery, but, from that time, they will no longer have to fear the virus. You have now imagined exactly what happened at the start of the age of immunization. The time was the mid to late 1700s, the place was the colonies that would become the United States, and the epidemic was smallpox, a dangerous disfiguring illness. One of the families involved, in 1776, belonged to John Quincy Adams.

At the time, there was no FDA to regulate the treatment, known as variolation (from the Latin word variola meaning spotted).  People risked contracting severe cases of smallpox from the treatment, but they chose to go ahead because smallpox was a fearsome disease which, for centuries,  swept through both the Old and New Worlds in epidemic waves, appearing and disappearing, killing millions, scarring survivors, and changing history as the scourge laid armies low on one side or the other.

An idea with a long history

The idea that suffering a mild case of smallpox prevented a severe case arose independently in several different parts of the world, with the first written reports dating back to the mid-16thC in China. Cotton Mather, a Boston preacher, learned of the practice of deliberate infection from his African slave Onesimus in 1721 and introduced the practice to the Americas. Infected material or scabs from smallpox pustules were inhaled or scratched into the skin and while the practice killed 2-3% of the patients, that toll was considerably less than the 30% mortality rate of the epidemic disease.

How the variola virus causes smallpox

Pustules are the distinguishing marks of the disease called smallpox. The variola virus, whose only host is the human, enters the body via the mucous membranes of the mouth and nose. The virus multiplies quietly inside cells, producing no symptoms for 10-14 days. Then the body reacts with high fever, headache, and malaise. Patients take to their beds and develop a rash – at first, red spots, but then blisters which fill with pus.  They spread from the mouth and nose, over the face, down the trunk and extremities. Coughing and sneezing spew infected material from pustules into the air, spreading the disease to caretakers. Deep skin lesions leave permanent pocked marks such as those scarring the faces of George Washington and Abraham Lincoln. Unlike many other viruses, variola is fairly hardy outside the body, which enabled its transmission from contaminated blankets given to native Americans by the British during the French and Indian war. The virus also traveled downwind from hospital ships on the Thames River in England in the 1890s.

The role of milkmaids in the history of immunization

The next chapter in the history of immunization occurred in Britain, where the fabled, beautiful skin of milkmaids was attributed to resistance to smallpox, conferred by prior infection with cowpox, a milder disease now known to be caused by the vaccinia (meaning cow) virus. In the late 1700s, Edward Jenner, a Gloucestershire physician, successfully prevented small pox by prior inoculations with the material from cowpox infections. The inoculations were called vaccinations, and Jenner became “the father of vaccination.”

Elimination of smallpox

The cowpox vaccine evolved over time into the standard vaccination procedure which eventually resulted in the elimination of the smallpox virus from the human population in the mid-1900s. The last natural case occurred in Somalia in 1977. Smallpox vaccinations, which had significant adverse effects in 1-2% of the population, were discontinued in the US in 1972 and the WHO declared smallpox eliminated from the world in 1980. Variola is the first and only virus to have been eliminated as a source of human illness, but other infectious diseases have been tamed in similar fashion and the hope is that new ways of creating vaccines will be even more effective.

How vaccines work

Smallpox vaccines were made from whole, live vaccinia viruses. Some vaccines for other diseases come from attenuated viruses (weakened viruses that transmit disease less effectively), or from killed viruses. Some vaccines are directed not at viruses, but at bacteria or at toxins like those produced by the diphtheria bacteria. All of them induce the immune system to create a memory of the specific organism or toxin, which will protect against future infection with the organism or the effects of a toxins like the ones produced by tetanus or diphtheria bacteria.

Because the immune reaction to infection is complicated and involves many types of immune cells as well as production of antibodies to the infecting organism, immunity to future infection is best induced and longest lasting after actual infection. Immunity after smallpox infection is lifelong, but lasts only 5-7 years after smallpox immunization. Other vaccines, especially those made from live organisms, are very effective and, some provide lifelong protection, especially with periodic booster doses. They have made infections like polio, measles, diphtheria, whooping cough and tetanus so rare that many doctors have never seen such illnesses.    

New technology

Like variolation, vaccines that rely on whole organisms can cause serious and unintended consequences. In the last two decades, genetic technology has enabled researchers to create vaccines from small parts of disease-causing organisms like COVID-19 or hepatitis viruses. Since sequencing genomes became automated and less expensive, the world of genetic virology and bacteriology has exploded. It is no longer necessary to rely on tedious and technically difficult culture methods to grow and identify microscopic and submicroscopic organisms. And it is possible to break down genetic information and use it to artificially produce components of these organisms or the proteins they produce, employing stock materials off laboratory shelves.

Using genetic material from viruses, researchers get living cells in laboratories to produce proteins specified by those genes and then create vaccines from the proteins. Or they inject the genetic material directly into people to get their cells to make the proteins. The immune system then recognizes these proteins as foreign and creates antibodies and memory cells against them. Theoretically, the induced immune memory prevents infection should the vaccinated person encounter the virus.  But much work remains. Some of the vaccines tried do not produce robust or long lasting immunity. Some have had paradoxical effects, with the immunized individual responding to actual infection with worse disease, as if a small amount of immunity actually enhanced the ability of the live virus to cause illness. The widespread deployment of the new COVID-19 vaccines – apparently effective in test groups over a relatively short testing period (safety studies in the past have run for years) will provide an enormous amount of information as to long-term safety and efficacy over years to come. This will be the largest and most public trial so far for the vaccine industry’s newest technologies. If the results are as good as the researchers who have developed them expect them to be, you can expect more and more vaccines to appear on the market.

 In the meantime, smallpox virus samples still exist in the US and in Russia. If these stocks had been eliminated, as once was planned, the smallpox virus would truly have disappeared from the world because, unlike most of the viruses that plague us, the small pox virus has no other animal hosts. And while there are long term plans to create new smallpox vaccines, it would be wise, in this uncertain world, to maintain the ability to rapidly understand the genetic makeup of the smallpox virus, as well as to rapidly implement old-fashioned smallpox immunization.

One-Footedness: The Key to Balance

Human beings negotiate the world on two legs, a skill mastered in toddlerhood. As children we are well balanced and swift. Then one day in mid-adulthood, we look at our children and realize that they are fast out-performing us in skills that require balance. When did balance become more difficult?  Of course we cannot define that point because life sneaks up on us, nibbling away at skills we do not practice because nature works assiduously to conserve energy.  Motor and mental tasks we do not practice get put to rest.

What’s involved in balance?

We maintain balance by taking in three types of sensory input and adjusting muscular activity accordingly. The three input systems are vision, messages from hair-like projections in three fluid-filled canals set at right angles to each other in the bone of the middle ear, and continuous reporting from delicately engineered receptors in our muscles and tendons that measure stretch and tension.  We can learn to balance without the first two components of the balance system, but not the third. To demonstrate the importance of the input from the muscles and tendons, try getting up and walking after one foot has fallen densely asleep from pressure on the nerves which are the highways for sensory information on its way to the brain. Even if you can wiggle the foot because motor nerves are more resistant to pressure, you cannot use it without knowing where it is.

Use it or lose it” applies to balance

Much of modern adult life involves little more than moving from one form of sitting to another, which gives the feedback systems in the eyes, ears, and muscles and tendons little exercise. Over time, balance skills deteriorate, and eventually falling happens with simply tripping or changing position or direction. Falling is the cause of many hospitalizations and, often, the injuries incurred lead to death. Living well and independently over the decades depends in no small part on maintaining the ability to walk without falling. Fortunately, balance improves with practice, and we have ample opportunity throughout the day to engage the balance systems and give them a workout.

Waking up the eyes and ears

Eyes are easy. Look around while you walk. Off to the side, up, down, straight ahead. If you are a straight-ahead looker most of the time, looking around may make you feel a bit unsteady at first. But your brain will begin to coordinate the changes with the information coming in from the ears and the muscles, so it will get easier. Once it does you can add more head movement, following your gaze. That will add more movement of the inner ear canals, which can become very accustomed to minimal movement. Young adults taking dance lessons for the first time or grandparents taking grandchildren on park equipment might be surprised to find themselves dizzy because of long unpracticed movements that involve spinning in circles or bending over. The ears are reporting unusual movements but with practice they will re-learn and stop sounding alarms. Deliberate exercises in head tilting and turning, such as the ones widely prescribed for benign positional vertigo, can speed the process.

Waken the muscle receptors by paying attention to walking

The stretch and strain receptors in the muscles are active whenever we are upright, but also lose function – even in walking, which is the most frequent and complex motor function we perform. Walking involves the subconscious coordination of over 300 muscles in a series of controlled falls that move the 200 bones of the skeleton forward or backwards in space, sometimes with the addition of upward or downward travel on stairs or ramps. Walking requires one-footed balance, with one foot bearing the body’s entire weight while the other foot swings forward. Landing the forward moving foot prevents the body from falling as it moves forward.

As the years pass, the body’s motor system tries to conserve energy by allowing you to use fewer, large muscles rather than more numerous small ones to accomplish the task of walking. Balance suffers and it is harder to adjust quickly to uneven terrain or surprises that throw you off balance. Learning to re-engage and strengthen all the smaller muscles devoted to one-legged balance re-awakens a lot of the sensory input and improves stability in all your upright activities.

Exercises for one-footedness

A good exercise for developing one-footed balance involves standing on one foot while barefoot (elevated heels throw the center of gravity forward), lifting the other knee in front of you and using a countertop for support. The gluteal muscles in the buttock on the side of the weight bearing leg will be forced to contract to keep the pelvis from dropping on the other side. The entire foot, powered by the lower leg muscles, is the stable platform that supports the rest of the body and the big toe stays in active contact with the ground. As strength and balance improve, try moving away from the support of the counter, getting the free knee up to a right angle in front of you and then swinging it down and back and a little behind you, concentrating on keeping the pelvis level and stable and the trunk upright. Adding toe lift exercises on stairs – dropping the heels a little below the stair level and pushing up from there – adds to the strength and flexibility of the ankles and to sensory input from the many intrinsic foot muscles and lower leg muscles.

Taking the exercises out for a walk

Once you get the feel of the muscle contractions necessary for one-legged balance, then try to feel the same sequences of activity while walking.  Good, upright posture helps. Your head weighs 10-14 pounds when directly over your spine, but the weight doubles, triples and even quadruples in proportion to how far in front of the body it is. If you have the habit of jutting your head forward with a curve in the back of the neck, or looking at the ground while you walk, the work of balancing increases proportionately. Keep the chest lined up over the pelvis and engage the trunk muscles – the so-called core – by trying to lift the pubic bone upward with the front of the abdomen. The core muscles maintain proper pelvic tilt. Then, while walking, try to feel the one-footedness you practiced while standing next to the kitchen counter and the ankle motion you felt doing toe lifts.

The action in walking is at the hip, ankle, and foot. The role of the knee is to let the leg bend as necessary. As you shift your weight to one foot, the gluteals contract in the buttock to hold the pelvis and prevent the released side from dropping. In the brief phase before the supporting leg begins to push you forward, notice the entire sole of the foot. Its connection with the ground begins with the heel planting down and continues as the body weight rolls forward. The knee will be straightest when you push through and are about to plant the new foot.

Do not neglect the feeling coming from the toes – especially the big one as you push off and begin to move the other leg through. Toes add a significant amount of surface area, increasing the available sensory information fed into the motor system and they contribute to the push phase of the gait. Notice also how the ankle moves as the heel lifts off the ground. Notice all of it as your other leg is swinging through and really try to relate the sensations to the one footed balance exercises you have done to practice.  

Notice other gaits

And while you are out walking and noticing your own one-footedness, take a look at some of the gaits you see. You will begin to learn the risk factors for falling. You’ll see people using only large muscle groups, initiating the leg swing by lifting the entire side of the body, from the shoulder down. They are already off balance. Their bodies must tip to the opposite side to allow the advancing leg to clear the ground. When the new leg lands and the weight shift begins again, the gluteals are not engaged, there is no push off from the hip and the foot, and the other side begins to lift from the shoulder. On a sunny day you will see such a walker’s shadow shift from side to side. Sometimes there are physical problems that impair walking balance, but for someone in good health, without neurological disorders like neuropathy, working to make the shadow move in a straight line pays off in a longer functional life. 

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