Drs. Randolph and Rea found that indeed almost everyone with a chronic degenerative illness had a portion of their symptoms linked to environmental sensitivities. Foods weren't the only culprit. In almost all cases the more common airborne allergens like dust, molds and pollens were also involved. Sensitivities to specific chemicals could also have profound effects. Things as seemingly insignificant as the chlorine used to disinfect tap water or natural gas emanating from a stove would have a sort of multiplier effect in making food sensitivities even worse. The ubiquitous use of solvents in paints and carpet adhesives coupled with formaldehyde in wood products, made poorly ventilated new office buildings a new source of illness.
The obvious question became why did some folks find these surroundings so toxic while others seemed to be relatively unaffected? Walt Stoll, M.D. gave the most eloquent explanation for the mechanism behind observed food, chemical and other airborne sensitivities in his book SAVING YOURSELF FROM THE DISEASE-CARE CRISIS. In it he describes how our intestinal tract offers the largest single source for antibody activation and the resultant inflammatory responses that we experience as symptoms. More importantly he explains the mechanisms that lead to this situation. Before examining that, we need to back up a bit and get a rudimentary understanding of how our immune system functions.
Our immune system creates antibodies whenever something foreign to it penetrates our protective shell. I use the term 'shell' here in a figurative sense to include both the structures that are inside our body (including our mouth, esophagus, stomach, intestines, colon, etc.) as well as the skin covering the periphery of the body. Our body also uses a variety of non-structural secretory systems to limit alien substances from entering the bloodstream. Examples of this type would include excess tearing of the eyes and greater production of mucous to cover the nasal tissues when exposed to a dusty environment.
Once a foreign substance penetrates these structural and secretory barriers for the first time an immune response is launched. Initially it involves fluids that clump the foreign substance together so that they can be more easily recognized and carried out of the body. A subsequent and more sophisticated immune response then takes place involving a certain type of cell (called a lymphocyte) that singles out the foreign substance. These lymphocytes are antibodies that are able to chemically adapt to fit and lock onto the structure of the invader. Once this happens a cascade of events take place. Other lymphocytes rush to attack, enzymes are released and hoards of new lymphocytes are bred (or cloned) to 'search out and destroy' that particular invader.
This cloning is the way our immune system develops a 'memory'. This memory is important since the next time this particular invader breeches our protective barriers our immune system will be prepared to launch an immediate and much more powerful response.
Immunological memory works on our side when we receive vaccinations. A good example is the flu shot. Fragments of a dead virus are injected and the body responds to this foreign antigenic material by creating specific antibodies. It's important to note that it's not necessary to inject the real virus, just some of the pieces, since they contain the protein chains that our antibodies use to identify the virus as an invader.
Our body responds with a mild immune response. The intruder is recognized but there are few antigens that have been created to attack it. We might experience weak symptoms of headache and slight fever as more antibody cells form and attack the virus fragments (which remember are dead). They proceed to clone themselves and multiply to prepare for a prolonged battle or a new infection.
Later when we are exposed to the real virus, we have a massive army of antibodies that are ready and waiting to stop the intruder in it's tracks. In essence we have 'tricked' our immune system into launching a more massive attack on the living virus, by introducing something prior (in this case dead protein chains) that only somewhat resembled the real thing.
This memory can also work against us. When someone is exposed to poison ivy for the first time there will be little if any consequence. However the second contact is a different story. The immune system has had the opportunity to employ it's 'memory' to manufacture specific antibodies to the poison ivy antigen which consequently results in a much stronger response.
The immune response starts a complex avalanche of biochemical reactions which, when given the right situation, can be much more toxic to the body than the poison ivy antigen would have ever been by itself. This example illustrates how the downstream cascade of biochemical reactions can almost be completely responsible for the severity of our symptoms. Remember, everything is initiated by the antigen/antibody reaction alone. If you don't come in contact with the poison ivy you won't have any symptoms.
The majority of rheumatologists perceive (and tell their patients) that rheumatoid disease is 'auto-immune' in nature. In other words they believe the body produces antibodies that turn on itself by attacking it's own tissues. This is true in the strictest sense, but what drives the production of these 'self' attacking antibodies is where the argument begins.
Some antibodies (in their early development) may actually be capable of reacting with 'self' tissues. Almost always these cells are killed or inactivated before they can do any harm. Rheumatology believes that due to some genetic defect that these self reacting cells are not killed. Rather they are allowed to clone an army of other self reacting antibodies that ultimately strike out against our own tissues.
THIS IS NOT WHAT IS HAPPENING. Instead antigenic material that is not routinely able to penetrate the secretory and structural barriers of the body is somehow finding it's way into tissues and then the bloodstream. This antigenic material comes from a variety of sources. Some that we've already described include poorly digested food proteins, chemicals and inhaled allergens. Others (that will be described later) encompass the world of all living micro-organisms.
Once formed, antibodies seek out the protein component of invaders that match their own molecular structure and subsequently lock onto and carry them out of the body. Unfortunately if any of our healthy tissues have a protein component that looks similar to those of the invaders our feisty antibodies will attack.
The protein backbones of these molecules don't even have to be that closely related. Stanford University researchers have found that the amino acid sequence of a virus only needs to be identical to a 'self' protein for 5 amino acids (the building blocks of all proteins) within a stretch of 10 amino acids in order to 'trick' the antibody cells into attacking the self tissue. In this case while the antibody is attacking the virus, many are circulating throughout the body and doing the same with 'look-alike' cells comprising healthy tissues.
Rheumatic fever dramatically displays this mechanism. Rheumatic fever is an inflammatory disease that can affect many connective tissues of the body — especially those of the heart, joints, brain or skin. It begins with a strep throat from streptococcal infection. The antibodies that our immune system has created to target that streptococcal infection begin launching an attack on healthy tissue. The resulting damage might lead to rheumatic heart disease which may last for life.
This might be more immunology than you ever wanted to know and the differences in point of view might seem subtle. Certainly the destructive results are the same. But it is important to understand that your rheumatologist believes that we are a 'sealed' system.
In other words that the driving force for producing these destructive self attacking antibodies is completely internal in nature. Something has gone awry, perhaps due to a genetic defect, but they don't know what it is. They just know that it, the immune system, shouldn't be functioning this way. Contrast this with the view that our immune system is indeed producing these antibodies, but the true driving force for their production is from sources outside the body.
Rheumatologists suggest the auto-immune response as being the result of a hyper-active immune system. Initially it is hyper-active. As you will find later, the floodgates have been opened allowing a massive onslaught of outside invaders. However folks with auto-immune disease will eventually become immuno-suppressed from the constant demand to address all these outside invaders. Over time their immune system will be even less capable of dealing with a variety of ever present opportunistic micro-organisms that were previously handled in a routine manner.
If auto-immunity is really due to a foul-up in the internal works of the immune system our only way of turning it off would be to use powerful immune suppressing drugs to numb or slow the process. The fact that you can turn the auto-immune process down, and back up again (without drugs), gives decisive proof that modern rheumatological thought cannot be correct. By controlling the flow of antigenic invaders into the body we can control arthritis.
Associating a rash on the same part of the skin that recently came in contact with an oily leaf (like poison ivy) seems fairly obvious. Connecting an anaphylactic reaction (where the response is so severe that breathing can stop) from a bee-sting on the toe is a little more difficult. Somehow a minute amount of antigen (from the bee stinger) can effect distant, unrelated tissues. We are still very much in the infancy of understanding the mechanisms involved with our immune system. Fortunately, getting stung by a bee and having breathing spontaneously stop are not common events in our everyday life, so we've been able to make the connection.
Unlike this example, the process that leads to our intestinal tract becoming the primary gateway for antigens into the body is usually a slow, cumulative process. It is not available for direct observation. Maybe this is why the relationship between a 'leaky' intestinal mucosa and rheumatoid disease has been so elusive to modern rheumatology.
Walt Stoll, M.D. not only saw the connection between a chronically 'leaky' intestinal mucosa and disease but found ways to reverse it. This enabled patients to turn their symptoms off completely or dissipate them to the point where they were much easier to manage. He spent over 20 years treating sufferers that, for all intents & purposes, other physicians had cast aside and deemed 'resistant to conventional therapies'.
Dr. Stoll found that these patient's bodies had become very 'resistant' to drugs that were solely targeted at suppressing symptoms. However once the mechanisms that led to 'leaky gut syndrome' were addressed, the primary obstacles to healing were removed and symptoms would resolve on their own. For the first time since becoming afflicted these patients were giving their bodies a chance to normalize, and in so doing, tap their innate healing powers.
Dr. Stoll was very familiar with the research work done by the eminent physiologist Hans Selye, M.D. Selye found that he could induce symptoms and ultimately chronic illness in his test animals if he exposed them to any of a wide variety of physiological burdens. These included such things as starvation, prolonged exposure to heat or cold, excessive muscular exercise, surgical injury or sub-lethal doses of drugs. It wasn't any surprise that these animals failed to prosper under such harsh conditions.
What was totally unexpected was that the symptoms induced in the animals were the same. They were completely independent of the type of burden (or stressor) placed on their system. In other words it didn't matter whether the animal was exposed to cold or a sub-lethal dose of a drug. The animal would predictably have the same physiological response and develop the same symptoms.
Prior to this Dr. Louis Pasteur had become famous for his work in developing what today is termed the germ theory. As you might know, before Pasteur's discovery doctors did not wash their hands before performing such tasks as surgery or the delivery of babies. Infections seemed an unpredictably fickle part of doing these procedures, probably brought on by demons and devils. Aided by the invention of the microscope, Pasteur was able to see a world teeming with micro-organisms and make the key connection to infectious disease.
Since Pasteur's discovery medical science has focused the great majority of it's energies in defining the vast array of microscopic organisms that interact with humans. Once these 'bugs' were isolated attention turned to creating antibiotic pharmaceuticals to help rid us of these invaders. The quest has continued to this day and unfortunately, in the process, dwarfed the badly needed research to understand the flip side of the coin.
The synthesis of these vaccines and antibiotics was undoubtedly of major importance. However the overwhelming focus of treating the micro-organism led to an out of balance view of our world. The adaptive and natural resistance abilities found in the animal (or host) were considered static and unchanging (or at least unchangeable). Laboratory research was much easier if medicine could make the (false) assumption that the immunological status of the animal was constant (a perfect control) while testing the effectiveness of various antibiotic drugs. For all intents & purposes, medical research neglected what was at least half of the picture.
If the importance of the natural resistance of the host (in this case human beings) hasn't occurred to you, yet you've probably fallen into the same trap as most of our modern medical practitioners. It's the erroneous belief that we can defend ourselves from any infectious invader, if we just have the right antibiotic.
You will find your physician can talk at length about any type of microbe and the proper antibiotic to treat it. Odds are excellent that if a patient has a malady their doctor 'will have a pill for it'. But, if you ask what you can do to help boost your innate immunity, a deathly silence will follow. Physicians have next to no training in this matter and their patients have suffered for it. Pasteur, who devoted his entire life to understanding germs, admitted late in life that he had only 'worked one side of the street'.
Let me point out that Pasteur was the first to declare that disease was caused by microscopic germs. Being the first he was sharply criticized by many of his enemies for failing to recognize the importance of the terrain (the soil in which disease develops). They accused him of being too one-sidedly preoccupied with the apparent cause of disease: the microbe itself. There were, in fact, many debates about this between Pasteur and his great contemporary, Claude Bernard.
As age draws us closer to a natural death, it becomes obvious that our natural immunological resistance is 'everything'. It is the true warrior and it has been all along. Antibiotics, vaccines and the like certainly have their place, but best used only to fill in the gaps.
Dr. Selye observed three levels of physiological response. Stage 1 (the alarm reaction) starts about 6 to 48 hours after an initial injury. It is characterized by a lowering of blood pressure, loss of muscle tone, and shrinkage of the adrenal glands as they pump out as much cortisone as possible. Selye also noted other symptoms such as swelling due to leakage of fluid from smaller blood vessels into surrounding tissues.
Stage 2 starts about 48 hours after the original injury. By now there was considerable enlargement of the adrenal glands and the previously seen swelling in the tissues (produced by the leakage of fluid from the blood vessels) started to subside. The pituitary gland, which controls virtually all the other glands in the body, produces increasing amounts of adreno-cortico-stimulating hormone which causes the adrenal glands to produce even more cortisone.
It was during Stage 2 that Selye observed when he applied further small, repeated doses of the harmful stimulus (be it an allergy producing stimulus or any other) the test animals built up a resistance. They had now seemingly become adapted to the stressor and showed no observable external symptoms at all.
If the rats in this adapted stage were removed from the harmful stress (for example a persistent cold stimulus) they lost their newly acquired resistance (or adaptation) to the cold within a few days. When re-introduced to the cold environment they had to once again go through the Stage I alarm reaction (with all of it's associated symptoms) before re-acquiring their 'adaptation'. Conversely, if the rats were left in the cold, they continued to adapt for a long time, and appeared (at least externally) to have grown completely accustomed to it.
Selye noticed that if the rats continued to be exposed to the cold for a longer time that they would start showing new external symptoms. This was Stage 3 and it seemed that the animals had exhausted their resistance and had now become 'maladapted' to their surroundings. There was no Stage 4. If these animals continued to be exposed the cold they would quickly grow very ill and subsequently die. During Stage 3, warming the cold environment a bit was not helpful. Only the COMPLETE removal of the harmful stimulus would produce a healthy animal again. The transition from the adapted to the maladapted/exhaustion stage was, clinically speaking, what doctors would describe as the start of chronic disease.
Selye (without knowing it) had witnessed and described the mechanism that Dr. Rinkel had found so painfully with his experience of 'masked' food allergy to eggs. With the long term ingestion of eggs Rinkel had moved to Stage 2 and a form of adaptation to the ongoing stress of antigenic material in his body from eggs. There was no initial alarm reaction since the build-up of masked food allergy is a relatively long process.
As this adaptation petered out and physiological exhaustion settled in, Rinkel experienced greater chronic nasal problems (rhinitis) characteristic of Stage 3. When the offending stressor (the eggs) were completely removed from Rinkel's diet for 5 days the rhinitis disappeared. However when the body was re-exposed to eggs he experienced a hyperacute response (falling unconscious) consistent with what Dr. Selye predicted as a Stage 1 alarm reaction.
While Dr. Stoll was teaching at the University of Kentucky School of Medicine he gathered data from the physiology lab showing the effect of exercise stress on various organ systems. While at rest the abdominal organs (stomach, small intestines and colon) exhibited the highest blood flow, but once even light exercise began, the flow to the heart, muscle and skin tissues grew geometrically. At the same time flow to the abdomen rapidly decreased. In fact the abdomen lost a greater percentage of blood flow than any other system when engaged with the slightest stress.
The reason for this response to stress is an inborn throwback to our ancient ancestors and has been labeled the 'fight or flight' response. Herbert Benson, M.D. (Associate Professor of Medicine at the Harvard Medical Schools gives the best description of the human reaction to stress in his book THE RELAXATION RESPONSE. This innate fight-or-flight reaction is well recognized in animals. A startled cat standing with it's back arched and hair raised is suddenly prepared to run or fight; a dog on the attack with dilated pupils, snarling at its adversary; a gazelle running from a predator; all are responding by activation of the fight- or-flight response.
We tend to think that we have lost this side of our being and replaced it with rational control. This is simply not the case. Benson's research showed that when faced with situations that require adjustment of our behavior, an involuntary response increases our blood pressure, heart rate, rate of breathing, blood flow to the muscles, and metabolism, preparing us for battle or escape.
Dr. Stoll recognized that any activation of this 'fight or flight' response would lead to tremendous loss of blood flow to the intestinal tract. Our ancestors millions of years ago would use this response to their advantage when needed and then quickly return to a relaxed physiological posture where normal blood flow would be restored. But a more chronic activation of fight-or-flight response is common in modern man where there is an abundance of lights, horns, ringing telephones and demanding work situations to trigger the reaction.
At the same time Stoll knew from Selye's work that ANY environmental burden would act on us as a stressor which would demand the physiology to make an adaptive response. The net sum of all this research pointed to the absorptive endothelium of the small intestines as the primary 'target tissue' that would have to bear the majority of the brunt of these involuntary physiological responses.
As mentioned before this intestinal lining has a high demand for cellular regeneration as it is replaced on the average of every 14 hours. If chronically starved for blood the intestinal tract will no longer do it's job perfectly. This in turn makes the ecology of the colon much more susceptible to the growth of disease-causing parasites which can damage the lining even further.
The stage has been set for 'leaky gut syndrome' with the subsequent transmission of all sorts of antigenic material into the body which can ultimately precipitate an autoimmune response.
You've probably noticed that none of the discoveries revealing the underlying mechanisms causing autoimmunity were coming from the field of rheumatology. In fact most of the early contributions were from physicians working with patients with psychiatric disorders rather than musculoskeletal problems. There was a very good reason for this phenomenon.
With the advent of the manufacture of the synthetic hormone cortisone, rheumatologists thought that they had finally conquered the terribly destructive symptoms of rheumatoid disease. The cortisone drugs were dramatically effective, at least initially. Most rheumatologists were convinced that this type of cortisone supplementation was required to offset a low or of inferior quality of natural cortisone production by their patients. They likened the situation to a diabetics need for more insulin. This excitement quickly faded when it was noticed that the extra cortisone would lose it's effectiveness over time.
Hormones in the body are regulated by internal 'feedback loops'. When excess synthetic cortisone is detected, the adrenals (which are responsible for making natural cortisone) responded by lowering their production. Over time the adrenal glands would actually shrink. This left the patient in an even more perilous circumstance. If they missed their daily dose of synthetic cortisone the body (now with atrophied adrenals) couldn't respond by making up the difference.
To make things worse, high doses of synthetic cortisone led to ulcers, weight gain, increased blood pressure, diabetes, premature cataracts and osteoporosis. Less obvious were the problems from induced immunosuppression. Cortisone drugs were an engraved invitation for opportunistic organisms (viruses, fungi, etc.) to multiply. Plantar warts could emerge. Any warm, moist areas of the body were especially prone to fungal infections.
By contrast the physicians working with mentally ill patients had no breakthrough drugs during this time. Psychotherapy was a mainstay but was ineffective for the vast numbers of patients with more severe problems. Most of these cases were institutionalized in mental hospitals.
These settings provided a unique opportunity for physicians. Doctors were forced to come to their patients to observe, diagnose and treat rather than the converse. More importantly the entire environment of the mental hospital was fairly consistent and could be controlled somewhat, especially when compared to the outside world. It was an extraordinary chance for doctors to have access to the entire climate of their patients and observe their goings on day or night.
Theron Randolph, M.D. made most of his discoveries while working at such mental institutions. His initial practice was limited to psychiatry. Once he observed the impact of environmental conditions (i.e. – foods, chemicals, inhaled allergens, etc.) on his patient's mental status he tried to share it with the psychiatric community and was summarily scorned for these new ideas. He decided he needed a better understanding of the field of immunology to help his patients so he returned to school and added this discipline to his medical repertoire'.
William Philpott, M.D. was another psychiatrist that made an impact in this area. Philpott initially resisted the idea that any type of allergy could be involved with the behavior of his patients. He had the good fortune to be exposed to many fine physicians in the field of allergy. They documented case after case showing such associations.
At the request of S. Klotz, M.D. (a physician that he held in the highest esteem) he read the works of Drs. Rinkel, Zeller and Randolph. The evidence was overwhelming. Finally he confronted himself with a decision. Should he dismiss these new ideas out of hand and rationalize that all these doctors were wrong, that they simply didn't understand enough about psychiatry, or should he let the evidence speak for itself? Once he overcame this hurdle he was able to make an enormous contribution into understanding the biochemistry of individuals suffering maladaptive reactions. His outstanding book BRAIN ALLERGIES outlined these important insights.
Dr. Randolph realized that the best medicine for his patients suffering from maladapted reactions was to simply avoid the offending substances. In most cases patients could immediately improve their environment (and their health status) by perhaps repairing their leaky gas stove, closing paint cans tightly, making sure bedding was dust free or removing moldy objects from the house. Foods however presented a different problem. We all have to eat.
Dr. Randolph would initially ask that all severe food allergens be completely removed from the patient's diet. Usually after three to six months of complete avoidance many patients could reintroduce these foods back into their diet on a limited basis. Unfortunately he found that his patients would very often develop sensitivities to new foods, almost anything, especially if it was eaten in a repetitive manner .
To avoid this dilemma he asked patients to eat as wide a variety of foods as possible and devised several 'spacing' strategies. He found if a food, say an orange, was only eaten once every four days, that the patient would probably avoid developing a sensitivity to it. This is the basis for what is now known as a 'rotation diet'. Foods are spaced apart by a minimum of four days for each rotation in a patients diet.
Some of the rules of the diet were quite elaborate. Randolph found that foods from the same families (i.e. oranges and grapefruit — both from the citrus food family) needed to be spaced. In other words since oranges and grapefruit fell in the same citrus family they should not be eaten on the same day. In fact if you ate an orange on Monday you should provide a space of two days before eating your grapefruit on Wednesday. Re-learning how to eat in this manner could be a challenge, but worthwhile considering the dividends of drug free relief of most of your chronic symptoms.
Dr. Philpott adopted these techniques and his patients experienced similar success. He provided important new research by making biochemical measurements of his patients, comparing them to healthy individuals. One significant discovery found that his 'maladapted' patients displayed abnormal amino acid profiles in contrast to those of the healthy control subjects. Amino acids are THE major building block for all cellular and chemical (including hormonal) activities in the body. Philpott perceived that if there were a prolonged shortage of these amino acid building blocks, that a vicious, degenerative biochemical cycle would ensue.
Food is mechanically broken down by the chewing action in the mouth. Enzymes are secreted at this time initiating chemical breakdown. The stomach generates hydrochloric acid to continue the process of turning the rather large food molecules into smaller molecules that can be more easily absorbed in the small intestines. Next the food heads through the duodenum where bicarbonate is released to turn the acid mix into a slightly basic pH. Here the pancreas excretes more digestive enzymes and the food proceeds to the small intestines for absorption. If everything works perfectly the protein portions of food will be completely broken down to it's smallest base molecule — the amino acid.
Philpott found that if his patients took amino acid and pancreatic enzyme supplements prior to eating as well as specific vitamins (primarily B-6, B-3 and C) that reactions to known food allergens would be lessened. This led him to believe that amino acid deficiencies were the major culprit in starting an ever increasing downward spiral of needed biochemicals. If amino acids were not available in adequate quantities there wouldn't be enough building blocks for the body to create more digestive enzymes (not to mention hormones, antibodies, and materials for basic cellular regeneration). If enzyme production was compromised, so would digestion (the process of converting large food molecules into amino acids).
With each digestive cycle the percentage of food broken down completely into amino acids would drop (due to the lack of enzymes). At the same time there would be an increased percentage of peptides (larger food molecules) that are the culprits inducing maladaptive food reactions. The body would also be systematically starved for certain nutrients. Mega-supplementation of the above appeared to be the obvious way to reverse this trend. The fact that this mega-supplementation did work somewhat was a key impetus for the multi-billion dollar health food supplement industry that exists today.
Generally speaking the basic, caloric food components fall into three broad categories — fats, proteins and carbohydrates. Fruits and vegetables are our primary natural carbohydrate sources. Dr. Philpott noticed that a high percentage of his patients had what was termed disordered carbohydrate metabolism or carbohydrate intolerance. His patients didn't seem to convert carbohydrates into glucose (a major energy source, particularly for the brain) in a manner consistent with healthy persons.
Philpott monitored the glucose present in the bloodstream at different time intervals following the ingestion of a test meal. Healthy individuals demonstrated a predictable pattern.
The first hour after eating, blood sugar (or glucose) levels would rise slowly and then peak. This corresponded to the time-line for the normal digestive process. On average it takes 30 to 45 minutes for food to reach the small intestines. After cresting, blood sugar started a gradual decline continuing throughout the next hour. At the end of this period glucose levels would come to rest very close to the initial fasting measurement (the level noted prior to the meal).
This decline in blood sugar was due to the release of insulin causing glucose to be moved from the bloodstream and into the tissues. Once there it would be transported across the cell walls and converted to useful energy. Finally, during the next 3-4 hours between meals, glucose levels would remain essentially stable. Stored glycogen in the liver and muscles provide a buffering effect during this time.
Most of Philpott's 'maladapted' patients demonstrated a diabetic curve or displayed just the opposite, a hypoglycemic blood glucose curve. The diabetic curve was characterized by a very large and rapid jump in blood sugar levels after ingestion of the test meal. Instead of cresting, the diabetic curve reaches it's peak and flattens out at that elevated level for several hours. The diabetic feels weak after eating since the energy potential from the glucose is locked in the blood and has trouble making it's way into the tissues where it can be used.
Conversely the hypoglycemic usually has a rapid rise and then a precipitous drop in blood sugar levels. Their blood sugar usually dips well below fasting levels within only hours after eating. The hypoglycemic can have a myriad of symptoms develop when this happens. We all need a modicum of glucose in the bloodstream to fuel the brain. The liver and muscles must hold sufficient glycogen that can be converted to energy and drawn upon in times of stress. The hypoglycemic lacks this reserve while the diabetic has difficulties converting this reserve into energy. Both diabetic and hypoglycemic tendencies put a huge stress on the human physiology.
Up until this time medicine considered these abnormal blood glucose curves as only being related to the ingestion of carbohydrates. Dr. Philpott discovered that these types of abnormal (and physiologically stressful) blood sugar reactions were not limited to carbohydrates. They could be evoked by foods of all types, including fats, carbohydrates or proteins. Petrochemicals would also induce abnormal sugar levels in susceptible persons.
Dr. Philpott hypothesized that an abnormal blood sugar curve was simply a general expression of some sort of undiscovered maladaptation. It added a tremendous, often hidden stress, to the physiology of his patients. It's important to reiterate that any form of maladaptation will, given enough time, express itself in chronic degenerative disease including arthritis, diabetes, mental disorders, etc. These can and do exist individually or in combination. Philpott had case histories of many patients that first presented with rheumatoid disease and then later with diabetes. He also observed cases where diabetes would be a pre-cursor for arthritis. The sequence of the appearance of these chronic diseases seemed to be dependent on the genetic make-up of the individual.


I want to take a moment to thank you for the excellent job you did on all my travel arrangements. Everything you arranged for me was done to perfection.
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NFT: The Next Big Breakthrough of the Universe
By Administrator August 6, 2021 0
Article Blockchain Non Fungible Token Technology Trending
Tags:BlockchainBlockchain TechnologyNFTNon-Fungible Tokens
Just in case if you are not aware of this, let us tell you. Almost half of 2021 has appeared to be the year of non-fungible tokens (NFTs). Believe it or not, NFTs took over the world. Prolific celebrities, athletes, and musicians are pouring almost all their creativity into the NFT space and its working. Although the NFT is in the nascent stage, there is so much excitement in it. On the other hand, the NFT marketplace is still yet to go in a full-swing. The idea of it had frozen over, leaving everyone second-guessing the NFT market – if it is going to be the multi-billion dollar market in the next five years or just go dead!
Well, after all the machine bots and enormous technology backups, thought art could never come back. But then, NFT changed everything. It has added new hope to artists and art lovers. Life is coming back to the tech & blockchain market.
"NFT weekly trade volume across the top NFT marketplaces surged 3,300% from the beginning of the year ($5.9 million) to its peak in February ($198 million) before diving 82% to $35.3 million in May. Since then, NFT activity has been grinding higher, reaching $78 million in transaction volume the last week of June, a rebound of 120% month-over-month."
NFT weekly trade volume across the top NFT marketplaces surged 3,300% from the beginning of the year … [+] DAPPRADAR, THEBLOCK
Source: DappRadar, TheBlock
The creators are working to build and make their communities stronger and layer incentives to energize the NFT space for them. Thanks to all those creators who are working to strengthen their NFT community and grow the entire NFT space.
Not just to sell or buy, but NFT has become a social status for each individual. It offers a badge to display on social media that conveys ones openness to the NFT community and the new technology. This will build social engagement, create awareness among other artists' communities and ordinary people. Like luxury brands and goods, high-value NFTs are beginning to benefit the cultures and embrace the communities and influencers. Recently, famous artist Mike Winkelmann, known as Beeple, smashed digital art records when his art piece was sold for nearly $69 million at Christie's. According to the auction house, this has positioned him "among the top three most valuable living artists," according to the auction house.
OpenSea is the world's largest digital marketplace for crypto collectibles and non-fungible tokens (NFTs). It is a great platform to buy anything from art to virtual reality, sports, and trading cards.
In June 2017, CryptoPunks was one of the first NFT projects that set the standard for the modern crypto art movement. The CryptoPunks of 10,000 (ever be minted) has unique traits with varying degrees of rarity algorithmically generated through computer code. Initially, they were released for free and could be claimed by anyone. But later, the high demand with secondary sales that exceeding millions of dollars for individual CryptoPunks. The CryptoPunk owners proudly display their avatars, symbolizing that they are the early adopters of the ethereum-based NFT ecosystem.
Jay-Z recently purchased a CryptoPunk and set it as a Twitter profile picture. This added significant credibility to the project and exposed to Jay-Z's three million followers for the first time. He brought it for 55 ETH, worth $126,000, on April 25.
Bored Ape Yacht Club (BAYC) is one such project again. The platform created 10,000 unique digital ape avatars that offer special access to owners, such as the digital graffiti wall called The BAYC Bathroom. This feature is only accessible to wallets that own at least one ape.
The Bored Ape Yacht Club (BAYC) is an NFT community that created 10,000 unique digital ape avatars … [+] BORED APE YACHT CLUB
The BAYC platform is also developing to provide unique features to each owner. Recently, the BAYC included fundamental changes such as clear intellectual property rights for ape owners. As a result, ape owners can create t-shirts or other merchandise with digital avatars linked to them. Hence, there will be no copyright infringement or any other legal battles for the owners.
Cool Cats is one more recent launch with 10,000 programmatically randomly generated cartoon cat avatars. It gains all the power and popularity with a unique body, hat, face, and outfit with 300,000 possibilities. Soon, they might also launch the possibility of breeding capabilities, monthly exclusive custom Cool Cat airdrops, merchandise giveaways, 3D cats, or cat comics. This indeed increases social engagement and strengthens the community with an increased market value.
So not just the digital cartoon avatars, but there is also a lot of content on NFT platforms. Paintings, music, digital creators, etc. NFT artist Mike Winkelmann, popularly known as Beeple, has launched WENEW, an NFT platform that curates and provisions iconic moments and powerful cultural artifacts. This represents him as an artist turning to an entrepreneur building a premier NFT platform.
WENEW's first auction memorializes tennis star Andy Murray's historic 2013 Wimbledon victory. The top edition provides the auction winner the chance to play tennis with Murray at the All England Club, two VIP tour experiences, and Centre Court tickets to the Wimbledon Gentlemen's Final in 2020, including various physical and digital memorabilia. The auction was completed, with the winner bidding $177,777 for the top edition.
As we see the potential of NFT, sooner or later, it would also have the artistic tribute to momentous historical events, celebrating sports and every moonwalk. The NFT space is excepted to grow and flow with greater user engagement and increased revenues. We will see more and more breakthroughs in the non-fungible token (NFT) market.

redpajama_set_name: RedPajamaCommonCrawl


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Payne: Driving down memory lane in the last Volkswagen Bug
Posted by Talbot Payne on May 21, 2019
Seventy years after it came to the U.S., the VW Beetle is retiring — for the second time (the first retirement came in 1978). The 2019 Beetle prowled the Penn State campus just as the first Beetles did when they took the country by storm in the 1960s. (Photo: Henry Payne, The Detroit News)
The Bug has been squashed. Again.
As the iconic Volkswagen retires from the U.S. market for the second time in 40 years, I spent a week driving down memory lane with the final model, the 2019 New Beetle. I took it to its American roots — a college campus — for my niece's Penn State graduation.
Stylish and peppy, my Final Edition front-engine Beetle has come a long way from the 1960s Beetles that captured America's youth. Simple and non-ostentatious, those so-called Type 1 Bugs were everywhere on university lots, the affordable first cars of generation Baby Boomer.
The 2019 Volkswagen Final Edition. (Photo: Volkswagen)
The tan 2019 Bug I drove was a curiosity at Penn State; it was a fashion statement that has outlived its fashion. It was also a gem, and its demise opens a flood of memories to late-boomers like me — as it surely did the early-boomers who mourned the passing of the rear-engine Bug in 1978.
Although other classics from the 1960s golden era of the automobile — Mustangs, Camaros, Challengers, Mini Coopers — have proved more sustainable than Beetle, it shares something with them. It's more than an automobile. It's part of the cultural fabric.
Detroiters mark decades by Tigers teams, couples mark sentimental occasions with favorite ballads. I mark my years with Beetles.
Lynn Anderson of Clinton Township stands by her prized possession, a 1965 replica of Herbie the Love Bug, in 2015. (Photo: Max Ortiz, The Detroit News)
My first memory of the creature is at the movies.
I come from a family of racers, and "Herbie the Love Bug" was right up our alley. When Herbie hit the screens in 1968, we were there. I adored the quirky car. It was the ultimate underdog among sleek competitors and the dastardly Peter Thorndyke.
I knew nothing at the time about the Bug's roots in Hitler's Germany. The Fuhrer's brainchild for an affordable "people's car" — hence, Volkswagen — was contracted to Ferdinand Porsche. Porsche himself was a difficult, mad genius whose rear-engine, bug-like design was the template for millions of Beetles to follow.
A couple cruises in a 1966 Volkswagen Beetle during the 2015 Woodward Avenue Dream Cruise near 9 Mile in Ferndale. (Photo: Robin Buckson, The Detroit News)
I doubt the students at Penn State who smiled at the passing Bug know its Third Reich history either.
That's because it was a Brit who ultimately brought the Bug to the world. In decimated post-war Germany, Hitler-partner Porsche (his son Ferdinand would ultimately start the sports car company that bears that name) was deemed by occupying American forces to be too radioactive to lead the company he started.
British Army Maj. Ivan Hiss rescued the Volkswagen factory and installed an executive team that would export Bug to the U.S. in 1949. It would become as American as apple pie.
Credit New York's Doyle, Dane, and Bernbach ad agency. With self-deprecating slogans like "And if you run out of gas it's easy to push," the Beetle was irresistible. It is featured in Paul Ingrassia's epic book, "Engines of Change," as one of the 15 cars (alongside the Model T, Jeep and Corvette) that changed America.
The title of Ingrassia's Bug chapter: "Volkswagen's long and winding road from Hitler's cars to hippie icons."
I didn't know many hippies as I came of age in the '70s, but I knew plenty of fellow 16-year-olds who cut their teeth on the Beetle. Bugs were as cute as Herbie. But man, that manual transmission saw some ugly shifting.
GROOOOONCH! The sound is still stuck in my head as my friends wrestled the shifter that grew from the floor like a cornstalk, mangling shifts as they worked the clutch.
"What's a clutch?" millennials might ask today.
My 2019 Bug is available only as an six-speed automatic, and it's smooth as silk. On a rainy weekend at Penn State, I would toggle Sport mode in the Beetle (an electronic gizmo that would be as alien to Ferdinand Porsche as hyperspace in Han Solo's Millennium Falcon) and shoot out of a green light, the automatic transmission effortlessly swapping cogs as the front wheels clawed at the wet payment for traction.
Front-wheel drive? The concept was as alien to the original Type 1 Bug as an automatic transmission.
By the late 1970s, governments were panicking over the OPEC-induced oil crisis and forcing manufacturers to make more fuel-efficient cars. VW developed the front-wheel drive, four-door Golf hatchback, which also happened to be more utilitarian than the two-door Bug and its cramped rear seat.
This 1967 Volkswagen Beetle was bought in 1966 in Riverside, California. Owner Kathleen Brooks has driven it more than 350,000 miles and recently had it restored. (Photo: Rick Loomis, Volkswagen)
As the Golf thrived, the Bug wilted. VW eventually put it put to pasture in 1978 (it continued production in Mexico until 2003 for foreign markets).
Then VW marketers heard the sighs of late-boomers like me.
In 1996, the Bug kicked off a Decade of Nostalgia that included retro redesigns of cars including the Mustang, Camaro, Mini, Ford Thunderbird and more.
Now a fashion statement instead of a mass-market car, the New Beetle was aimed at women, complete with dashboard flower vase and bright colors right out of my wife's spring dress collection. The New Beetle was still affordable and sold well initially. Ironically, it was based on the Golf chassis that had killed the original Type 1.
The New Beetle also shares the Golf's peppy 2.0-liter, 174-horse turbo-4, a long way from the Type 1's 30-horsepower hamster wheel.
But for all its Golf underpinnings, the New Beetle is unmistakably a Bug. Everything is cute and round: headlights, fenders, shifter base, speakers.
The New Beetle could never expand its female demographic to us motorhead males, though goodness knows the carmaker tried. I took a bright-yellow and black New Beetle to the race track known as the Autobahn in 2014. Dubbed the "Bumblebee" – a Bug with a stinger – it was stuffed with the Golf GTI's 210-horse four-banger. It was a blast. But what motorhead would pass up a GTI for a Bumblebee?
Dressing it in Herbie's red and blue racing stripes and No. 53 might have been a better idea.
A VW Beetle Cabriolet is shown in 1949, the first year Beetles were sold in the U.S. (Photo: Volkswagen)
And so the second-generation New Beetle has come to its natural end. With leather seats, sunroof, push-button start and modern gizmos like blind-spot assist, the 2019 Final Edition is a bargain at $26,000, just like its grandfather. Get it while you can.
Five years ago, on the Beetle's 65th anniversary, I test-drove a 1949 Type 1 Beetle, one of the first of its kind sold in the United States. For $1,268 new, it had roll-up windows, no air-conditioning and non-adjustable cloth seats. Zero-60? 28 seconds. Top speed? 68 mph. It's hard to imagine these things once were ubiquitous on American roads.
And it's also hard to imagine American roads without them. So long, Bug. Something tells me we'll see another version of you someday.
Jerry Adams, 3, plays with a toy Volkswagen Beetle while his dad's 1973 convertible Super Beatle is parked behind him in Bloomfield Hills during the Woodward Dream Cruise in this file photo from August 16, 2008. (Photo: Elizabeth Conley, The Detroit News, File)
Website Copyright © 2009 Henry Payne


A team of archaeologists found the remains of ancient naval base on the coast of Athens, Greece, which has an estimated age of 2,500 years.
In collaboration with a team of Greek, a Danish marine archaeologists, Bjorn Loven of the University of Copenhagen discovered the remains of six ship sheds. These ship sheds are used to protect ships from wood-eating marine mollusk (shipworm). These sheds also protect the vessels from drought while not sailing at sea. The sheds are found in Zea Harbour Project, which lasted from 2001 to 2012.
At the website of University of Copenhagen, Loven said his team analyzed the relics of glassware and did the carbon-14 tests on the pieces of wood. As a result, the ship sheds are estimated to stand at around 520 to 480 BC.
Not only that. The sheds are also believed to have used to stop by the ships that used the Greek army to fight against the Persians in the Battle of Salami, circa 480 BC. The war between the combined forces of the cities of Greece, led by Themistocles, and the Persian Empire led by King Xerxes.
Although outnumbered, the Greeks won, the war that took place in the strait between mainland Greece and the Salami islands. Their struggles have been adapted into a colosal movie titled, "300: Rise of an Empire".


Matplotlib is a powerful graphing and visualization library in Python. This tutorial aims to give users an introduction into graphing various types of data sets using the matplotlib library. Additionally, it will provide a cursory-level introduction of other easy-to-use visualization-based Python libraries, such as seaborn and pandas (for visualization only), that utilize matplotlib on the backend.


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Gay Men's Chorus Drowns Out Hate In Protest Of HB2 And The Orlando Massacre
With dignity in the face of bigotry and hate, the Triangle Gay Men's Chorus and the the Gay Men's Chorus of Washington performed in Raleigh, NC alongside an anti-LGBT protest nearby.
Posted on June 19, 2016, 22:58 GMT
Alex Matsuo Community Contributor
View this post on Facebook
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Which is Louder: Love or Hate?
On Saturday, June 19, 2016, the Triangle Gay Men's Chorus and the Gay Men's Chorus of Washington performed pop up concerts around Raleigh, North Carolina in protest of the recently passed House Bill 2, better known as HB2. Of course, with any protest, there are sure to be two sides of the spectrum. Along with the duo gay men's chorus, there were also anti-gay protesters nearby to ensure that their voices would be heard also.
In attendance was local Raleigh resident, Elizabeth Breakey, who took a video of the two forces coming together. In a mixture of love and hate, the gay men's chorus began to sing "Make Them Hear You" from the 1996 musical, "Ragtime." While they sang, the voices of the anti-gay protesters can be heard quoting scripture, likely from Leviticus.
Miss Breakey had her phone in hand and took an incredible video of the incident where the blend and combination of the two chorus' voices seem to drown out the speech just 30 feet away.
Miss Breakey described the moment on her Facebook page in the video description:
"This particular moment in Moore Square was one of the most amazing things I've experienced. As the choir began to sing, anti-gay protesters, about 30 feet away, started to scream out their hateful rhetoric, demanding the deaths of LGBT people in accordance with their God's laws. I've never heard such blatantly violent hate speech. I was in tears. And yet, these brave men stood directly in front of them and performed with pride, courage and conviction a song that perfectly sums up the battle.
After such a horrible week, where anti-gay hate-speech and legislation created a monster who murdered 49 men and women, it's a beautiful thing to see people stand up with courage in front of those that would see them dead and sing with kindness in their heart."
The video has already reached thousands of views and growing.


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Кязым Коюнджу (, 7 ноября 1971 года — 25 июня 2005) — турецкий музыкант лазского происхождения, уроженец города Артвин, Турция. Исполнитель лазского фолк-рока и автор песен.

Биография
В 1993 году основал фолк-рок группу Zuğaşi Berepe («Дети моря»), но в 2000 году она распалась. После этого Кязым приступил к записи двух сольных альбомов — Viya! в 2001 году и Hayde в 2004 году — которые оказались чрезвычайно популярными в Турции и Грузии.

В возрасте 33 лет Кязым умер от рака лёгких.

Дискография

В группе — Zuğaşi Berepe
 1995: Va Mişkunan
 1998: İgzas
 1998: Bruxel Live

В группе — Grup Dinmeyen
 1996: Sisler Bulvarı

Сольные альбомы
 2001: Viya!
 2004: Hayde
 2006: Dünyada Bir Yerdeyim

Рок-музыканты Турции
Рок-музыканты XX века
Умершие от рака лёгкого

redpajama_set_name: RedPajamaWikipedia


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Review – Fortnite
Kane Dane May 5, 2022 Fortnite
With 98% of the world's population having vanished and monsters suddenly popping up out of weird purple-hued energy storms, what's a Hero to do? If you're one of the 115+ Heroes in Fortnite, you build some sort of shelter, craft up a few guns and some ammo, then start wiping out enemy hordes – preferably in a group with three of your friends.
Fortnite is kind of hard to pin down, though Epic Games' claim that it's an "Action Building" game seems a decent start. Alone or in a team of up to four players, gamers will scour the procedurally generated map to gather resources by searching objects or breaking them down into their component parts, rescue survivors, and locate the objective.
Gathering resources makes the game feel a bit like Minecraft, and a whole lot like the recent plethora of survival games to hit the market. Smashing cars, trees, and rocks (among a slew of other objects) gamers gather up material to craft walls, floors, traps, and – most importantly – weapons. Schematics, used to craft new items, can be found in the environment or earned via quests, and can be leveled up using experience chips to produce more powerful weapons.
Fortnite features a massive roster of potential Heroes, though they'll need to be unlocked via quests or earned from the Llama piñatas that stand in for loot boxes. Heroes come in one of four classes: Constructor, Ninja, Outlander, and Soldier, with each having a unique skill. Constructors build/demolish faster, for example, while Ninjas can double jump. Subclasses like Recon Scout (Ninja) or Warlord (Soldier) providing additional variety to the skills they'll bring to the battlefield. Heroes can also be leveled up to provide higher stats and unlock new skills.
There are a variety of missions, but they tend to boil down to a few basic steps: explore the map to gather resources, scout out the location, and find survivors, then spend a few minutes to fortify the mission zone, and finally start the waves of enemies you'll need to mow down in order to succeed. Do well enough and you'll earn high level loot chests after the smoke clears, providing a satisfying end to missions and keeping you hooked for 'just one more' until it's the early hours of the morning.
Fortnite feels a little easy to start, especially when playing with a group, but it doesn't take long before you leave the starter zone behind and hit some real opposition. By the time you hit the third zone it's time to have a solid plan in place before summoning the Husk invasion, including fortifications that have had some thought lent to their construction. Sniper towers are a bonus if the team has a couple people with steady hands, but you'll have to adapt to the weapons people want to play with. After all, if you get a legendary shotgun it'd be a shame not to use it…
Though it's been released as an Early Access title, leading up to the game's full release as a free-to-play title next year, Fortnite feels remarkably polished with only a few instances of lag to detract from the action thus far. The game is undeniably more fun when playing with friends, as the solo experience can start to get repetitive – at least through the initial zone, which is more or less the training and tutorial area, albeit one with hours of content to churn through. The game looks great already, with a simplistic style to it that evokes Plants vs Zombies, and the performance has been solid outside of a few spots of lag. The third-person shooting mechanics are flawless, with my only wish being for a grenade toss indicator of some kind.
Insider: Fortnite will soon be transferred to the Unreal…
Fortnite Returns Short Film Festival - review Addiction
"Free Fortnite!" Schoolchildren broke into court between…
Epic Games Extends Season Two of Fortnite Chapter Two for &…
Fortnite - First Tutorial Mission Secret Loot and Easter…
Epic Games will give in-game currency to Fortnite and Rocket…
Let the force be with you! The list of the most successful games under the license of "Star Wars" in the USA is revealed
Christopher Nolan Films Shown At Fortnite This Friday – review


Search a .COM.DE domain name for your business or website at just 11.00 from ZNetLive.
.com.de is the country code top-level domain for the Federal Republic of Germany.
Why register a .COM.DE domain with ZNetLive?
Order your .COM.DE domain names in Bulk, simply enter your names below (one domain per line).


Aisi Deewangi MP3 Song by Alka Yagnik from the movie Deewana- Hindi. Download Aisi Deewangi song on Gaana.com and listen offline.
Aisi Deewangi Dekhi Nahi . episode 4 - may 25, 2017 . mp3wifi.link is a music search engine from where you can download your favourite songs from our Mp3 .


In June of 2014 I asked FC Dallas president Dan Hunt, who was a key figure in America's bid to land the 2022 World Cup, if the U.S. should get that bid in light of reports then that Qatar had bribed FIFA officials.
We now know for certain that the 2022 bid was bought, and the event should come to the United States ... where it should have been in the first place.
It had been rumored and alleged that the World Cup bids to Russia and Qatar were both achieved on bribes and kickbacks, which Wednesday's charges confirmed. If these charges, and realities, do not force FIFA and the international business community to change the destination of at least the '22 World Cup we should all quit.
The '18 WC in Russia is too late to change, but there is plenty of time for 2022 to be moved. The human rights' violations and atrocities going on with the construction in Qatar for the World Cup will convince you that absolutely no progress has been made in the last 100 years.
This bid should go to the United States, which has all of the necessary facilities and infrastructure to host another World Cup. Not nearly as many bribes will be required to make this happen. AT&T Stadium should host a World Cup match or two, possibly even the Finals.
"We were the one that was supposed to get that tournament," Hunt told me in that interview; both he and his brother Clark were active in the Dallas and North Texas to help with the U.S. bid for the '22 tournament. They were convinced the U.S. was going to get one of those two bids.
This just shows the giant stones on FIFA; while it knows a bunch of leaders and execs are going to take the fall, and it will be fined millions and millions of dollars, it's not going to change the way it sells its most lucrative prize - the World Cup.
All of these WC bids, which include South Africa ('10), Brazil ('14), and now Russia and Qatar, were all bought, and Wednesday's news confirmed the voting process as a sham.
Take the pretense out of it, and put the World Cup on the auction block like an antique painting at Christie's. Or just call FIFA a pimp, and the World Cup its best-looking whore.


If you get into a collision, you should talk with a car accident lawyer for help proving how the accident happened. If you can show fault, you should be able to get compensation. Unfortunately, it can be complicated in some cases to prove the other driver was to blame and thus should be held liable to you for losses. Brandon L. Lettunich, Attorney at Law can help victims throughout El Paso to prove their case by using expert witnesses, along with other available evidence.
There are many different kinds of expert witnesses who could potentially help you to prove fault in a car accident claim. A car accident lawyer can help you to determine what kind of expert you might need. One option is to hire an accident reconstruction specialist. They can assist in painting a picture of exactly what happened and what behavior led up to the crash occurring. You could also hire an engineer or an expert in road or vehicle design. This option is available if you are alleging that a problem with the road or a problem with the car either caused the collision. to occur or contributed to making your injuries worse than the injuries should have been.
A car accident lawyer does more than just help you to determine which expert witnesses to consult. An attorney can also help to make sure the witnesses are prepared. Witness prep is an important part of the process. Its main focus is making sure witnesses explain things in a way that the jury is able to understand. A car accident lawyer can also help you to try to make the jury doubt the testimony given by defense experts. This may also be introduced to cast doubt on the case you are trying to present.
In sum, if you have been in an El Paso car accident, you should contact Brandon L. Lettunich, Attorney at Law for assistance. Our legal team understands how to put together the strongest case possible with expert witnesses and other kinds of evidence. Contact Brandon L. Lettunich, Attorney at Law today to find out more.


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Q: Opencv get accurate real world coordinates from 2 known parallel planes So I have been tinkering a little bit with opencv and I want to be able to use a camera image to get the position of certain objects that are lying flat on plane. These objects are simple shapes such as circles squares etc. They all have the same height of 5cm. To be able to relate real world points to pixels on the camera I painted 4 white squares on the plane with known distances between them.
So the steps I have been taking are:
Initialization:

*

*Calibrate my camera using a checkerboard image and save the calibration data.

*Get the input image. call cv::undistort with the calibration data for my camera.

*Find the center points of the 4 squares in the image and pass that data and the real world coordinates of the squares to the cv::solvePnP function. Save the rvec and tvec return parameters.

*Warp the perspective of the image so you can get a top down view from the image. This is essentially following this tutorial: https://docs.opencv.org/3.4.1/d9/dab/tutorial_homography.html

*Use the resulting image to again find the 4 white squares and then calculate a "pixels per meter" translation constant which can relate a certain amount of difference in pixels between points to the real world distance on the plane where the 4 squares are.

Finding object, This is done after initialization:

*

*Get the input image. call cv::undistort with the calibration data for my camera.

*Warp the perspective of the image so you can get a top down view from the image. This is the same as step 4 during initialisation.

*Find the centerpoint of the object to detect.

*Since the centerpoint of the object is on a higher plane then where I calibrated I use the following formula to correct this(d = is the pixel offset from the center of the image. camHeight is the cameraHeight I measured by using a tape measure. h is height of the object):
d = x - (h * (x / camHeight))

So here for an illustration how I got this formule:

But still the coordinates are not matching up...
So I am wondering at all if this is the correct. Specifically I have the following questions:

*

*Is using cv::undistort before using cv::solvenPnP correct? cv::solvePnP also takes the camera calibration data as input so I'm not sure if I have to pass an undistorted image to it or not.

*Similar to 1. During Finding object I call cv::undistort -> cv::warpPerspective. Is this undistort necessary here?

*Is my calculation to correct for the parallel planes in step 4 correct? I feel like I am missing something but I can't see what. One thing I am wondering is whether I can get the camera height from opencv once solvePnp is done.

I am a newbie to CV so If anything else is totally wrong please also point it out to me.
Thank you for reading this wall of text!

redpajama_set_name: RedPajamaStackExchange


When I was servicing computers, the most common problem was a broken power plug. Here is a tip on how to fix a broken power plug in a Computer. First disassemble the computer and locate the wires going to the existing female plug. Next cut the wires going to the plug and attach 2 heavy wires with a good connection…. solder if possible. Remember to note polarity of wires, let wires out of computer via some gap or hole. Reassemble computer. Now attach those two wires onto any plug. I used an old plug from under the dashboard of an old car. Connect the matching male plug to the end of the original computer power supply…. being careful to note polarity. Your done… it may not be pretty, but it will likely never fail you.
Wow looks sort of crude.
The older straight plugs were bad for that. The newer laptops now usually have "L" plugs and don't break when banged against the wall.


There is still concern regarding potential health effects of nano-sized and nano-structured materials (NMs). Since reliable risk assessment is essential for sustained societal acceptance, there has been substantial funding for toxicological studies in the past decades. Albeit a wealth of data has been published since, the relevance of those data for risk assessment can be questioned. This is particularily the case for data from studies that focused on inhalation as the route of exposure. The derivation of exposure limits for NMs is still an elusive issue, although some regulatory measures have been undertaken e.g. for inhalation of carbon nanotubes at the workplace .
Today, one of the main obstacles for risk assessment of nano- and micronsized particles and fibres is not the lack of toxicological data, but a shortage of data meeting all of the criteria for use in risk assessment. One of the most important criteria is accurate dosimetry. While most studies provide accurate data on particle exposure concentration, i.e. mass of particles per volume air (μg/m3) or – for in vitro submerged cell-based assays – per volume cell culture medium (μg/cm3), the pivotal role of dose delivered to the site of exposure (e.g. lung epithelium (in vivo) or lung cell culture (in vitro)) has been widely overlooked. This is especially the case in - but not limited to - studies with in vitro cell systems [2, 3].
In addition, the choice of consistent and relevant dose metrics (e.g. mass, volume, surface area, number) has also been identified as one of the key issues for limited applicability of toxicological data for risk assessment . While this is beyond the scope of this editorial, we mention that current results indicate that – in addition to mass, the traditionally used metric – at least one more dose metric should be used such as surface area, volume or number, depending on the type of NM [5–7]. This editorial highlights the fundamental role of delivered particle dose (sometimes also referred to as internal dose) for translation of toxicological dose-response data into risk assessment and exposure limits. The concept of delivered dose is of overarching significance for any type of particle exposure scenario. For simplicity we are focusing on poorly soluble particles (PSP) and models for respiratory toxicity assessment, i.e. inhalation exposure for in vivo studies and cell culture exposure under submerged or air-liquid interface conditions.
Often, exposure is considered an acceptable measure for dose in hazard and risk assessment studies. One of the reasons for this false perception lies in the different perspectives on risk taken by the regulatory body and the toxicological community. In contrast to exposure concentration, delivered dose is often difficult to measure and real-time dose measurement devices are often not available at all. For practical reasons, regulatory measures of health protection have to set limits based on readily measurable quantities of exposure, namely exposure concentration levels ("exposure limit"). Ideally, these exposure limits can be adjusted to any substance by determination of material-specific hazard factors. This concept of hazard-based risk assessment is often presented in a simplified form describing risk as a function of exposure and hazard (risk=f[exposure, hazard]). However, this is misleading, since exposure to an aerosol of PSP is a poor predictor of delivered dose (see Fig. 1) and from a toxicological point of view only the delivered dose, i.e. the dose which comes into contact with an organism, can do harm. For inhalation the dose of PSP is strongly dependent on many factors including respiratory parameters (tidal volume, breathing frequency) and PSP-lung deposition which depends on PSP characteristics affecting the diffusive (mobility) and aerodynamic behaviour of PSP (size, density and shape) . Hence, the relevant measure for toxicological dose-response analysis with relevance for human risk assessment can only be delivered dose – not exposure. For definition of exposure limits, dose-based toxicological results have to be translated into equivalent exposure limits as described below.
As mentioned above reliable risk assessment of PSP hinges on (delivered) dose-response relationships mostly obtained from animal inhalation experiments. Derivation of dose-based Low or No Observed Adverse Effect Levels (LOAEL/NOAEL) and related human exposure limits require extrapolation of LOAEL/NOAEL from animal/cell to human conditions taking into account aerosol processing mechanisms and factors determining the relationship between inhaled concentration and delivered dose (see Fig. 1) [9–11]. Importantly, inter-species dose conversion (allometric scaling) requires appropriate normalization of the delivered dose. For inhaled PSP this is typically done based on mass of the lung or surface area of the lung epithelium (in vitro: surface area of cell culture system), i.e. ideally the normalized delivered dose should be presented in terms of μg/cm2-tissue (lung epithelium) or μg/g-lung (e.g. wet lung weight of mouse and rat vary around 0.18 and 1.3 g, respectively . It is noteworthy, that allometric scaling is often based on body weight, but for inhaled substances surface area (or mass) of the lung is more relevant than body weight .
Due to practical reasons most animal inhalation studies report dose-response relationships and NOAEL/LOAEL in terms of retained dose, i.e. delivered dose corrected for PSP clearance from the lung due to mucociliary and macrophage activity . To the best of our knowledge, it has not been investigated whether delivered or retained dose of PSP is more predictive for adverse health outcome. For humans and commonly used animal models the PSP clearance rates are well known and incorporated in computational dosimetry models (e.g. ICRP, MPPD) allowing for easy conversion from delivered to retained dose, if the exposure regiment (timing) and rate of delivered dose are known [13, 14]. Hence, at this time both delivered and retained dose are acceptable, but should be clearly identified and all parameters for conversion into each other should be documented.
As a consequence, derivation of human exposure limits from toxicological studies relies on dose-response data in terms of normalized delivered dose, not in terms of exposure. In other words, exposure-response curves in animal or cell models do not allow for direct conclusions on human exposure limits, i.e. for any toxicologically equivalent normalized dose the corresponding exposure levels in animals and humans are different (Fig. 1).
Historically, mainly in vivo animal studies were used for derivation of exposure limits and hazard factors, while in vitro cell models mainly contributed to identification and understanding of toxicological pathways. With the advent of more complex in vitro models of the lung and other organs, as well as from the perspective of the 3R principles of more ethical animal testing (calling for refinement, reduction and replacement of animal testing), in the future a more significant role of in vitro testing for risk assessment of particles and nanomaterials can be expected.
In principle, two types of in vitro particle exposure systems can be distinguished. Either aerosolized particles are deposited directly onto cell models of the lung cultured at the air-liquid interface (ALI) or particles are suspended in cell culture medium and incubated with cells under submerged culture conditions, i.e. cells are completely covered with particle-laden cell culture medium. Clearly, ALI exposures are mimicking the physiologic conditions in the lung more realistically and are therefore potentially more predictive for inhaled particles [12, 15]. Moreover, under ALI conditions the (normalized) delivered dose can be either determined directly using e.g. quartz crystal microbalances (QCMs)  or predicted by computational or semi-empirical aerosol deposition models taking into account all relevant aerosol properties and the experimental characteristics of each exposure system [13, 14]. On the other hand, exposures under submerged conditions are relatively easy to perform by just adding a known amount of PSP to cell culture medium. However, this is deceiving, since a substantial amount of effort has to go into preparation of stable particle suspensions and – even more problematic – into determination of the fraction of the administered dose (dose added to the medium) which is finally delivered to the cells [17, 18]. In the past, the preference of delivered dose over administered dose has been largely ignored or overlooked and only recently practical tools for determination of the (normalized) delivered dose in submerged cell systems have been presented [19, 20]. However, validation of these dosimetry models is hampered by uncertainty if cellular uptake of PSP is required for toxicological response or if contact between the cell membrane and PSP may be enough for stipulating toxicological response. Nevertheless, particokinetics models or cellular uptake/delivery measurements are currently recommended for estimation of the delivered dose.
To avoid uncertainties with particokinetics models, the delivered dose should be measured directly. In principle this is easily possible for in vitro air-liquid interface cell exposure experiments (e.g. QCM) and somewhat more complicated for in vivo animal and submerged in vitro cell experiments, but material-specific limitations may apply e.g. for carbonaceous PSP, which are difficult to detect in (carbon-dominated) biological matrices. Alternatively, the delivered dose can be inferred from the exposure concentration and particle deposition models, if a set of five to seven parameters is known, which depends on the type of exposure scenario as presented in Fig. 2. In all of these scenarios, the exposure concentration is multiplied by the volume of air (or cell culture medium) to calculate the administered dose which is subsequently converted into delivered dose utilizing particle-lung deposition models for animal inhalation experiments or particle-cell deposition (particokinetics) models for in vitro studies with air-liquid interface or submerged cell culture systems. For all of these three exposure scenarios the main PSP deposition mechanisms are typically diffusion, sedimentation, interception (relevant for high aspect ratio PSP) and/or impaction as well as electrophoresis and thermophoresis for some air-liquid interface cell exposure systems [12, 21]. Any of these processes can be described using a set of parameters related to either the exposure system or PSP characteristics, namely particle size, shape and density (plus electrical net charge for electrophoresis). It has been shown that these three PSP parameters can be lumped into two directly measurable parameters referred to as volume-weighted (median) equivalent mobility diameter and effective mobility density (ratio of PSP mass and equivalent mobility volume (= π/6 d m 3, with d m = equivalent mobility diameter) . For easy and reliable particokinetics modelling, both equivalent mobility diameter and effective mobility density should be stable during the entire exposure period. As mentioned above, in addition to these particle characteristics, three to five exposure-related experimental parameters have to be reported depending on the exposure setup as specified in Fig. 2.
Delivered dose – not exposure concentration - is absolutely crucial for consistency, risk assessment and regulatory relevance of inhalation particle toxicological studies, since it allows for inter-comparability between in vivo and in vitro data, read-across analysis (prediction of effects of the same (or similar) chemical entity with varying physical characteristics), and extrapolation of cell or animal data to human exposure conditions and subsequent conversion to exposure limits.
Cell/lung delivered PSP dose should be determined and normalization of dose to cell/lung surface area is essential for extrapolation of dose levels from cell culture or animal models to humans.
In addition to mass, which is still the most relevant metric for regulatory purposes, a biologically more relevant dose metric should be chosen. For non-fibre-specific toxicity, BET surface area seems to emerge as the most promising metric, but no final recommendation can be made at this time.
If only concentration instead of delivered dose can be provided, sufficient physical characterisation of the PSP and the experimental conditions has to be provided to allow for conversion from concentration to dose (see Fig. 2).
○ All relevant experimental parameters for conversion of particle concentration (μg/ml-medium) into administered dose (μg/cm2-cells) should be reported, namely exposure concentration in cell culture medium and medium filling height (derived from cell covered area and medium volume per well) (Fig. 2).
○ State-of-the-art methods should be used for conversion of administered to delivered dose and all relevant experimental parameters for conversion of administered to delivered dose should be reported . Currently, the most widely used set of parameters is volume-weighted equivalent mobility diameter and effective mobility density (ratio of mass and mobility-diameter-based volume assuming spherical particle shape) (Fig. 2).
The authors wish to thank Dr. Wolfgang G. Kreyling for his valuable suggestions. This effort was partially supported through EU Horizon 2020 project SmartNanoTox, grant agreement No. 686098.
OS conceived this editorial statement and wrote the manuscript. FC carefully revised the manuscript and made conceptual and editorial contributions. Both authors read and approved the final manuscript.
Lenz AG, Karg E, Brendel E, Hinze-Heyn H, Maier KL, Eickelberg O, Stoeger T, Schmid O. Inflammatory and oxidative stress responses of an alveolar epithelial cell line to airborne zinc oxide Nanoparticles at the air-liquid Interface: a comparison with conventional, submerged cell-culture conditions. Biomed Res Int. 2013; doi:10.1155/2013/652632.


For over 20 years Michael Shayne Durden burglarized hundreds of homes across Collin and Dallas County. He has spent his life learning how to break into homes to find and steal thousands of dollars worth of possessions. He was getting away with it until the Allen Police Department in cooperation with the Plano Police Department caught him. He is facing 20 to 30 years in jail.
Even though the serial burglar is remorseful, and provided valuable information in the interview, Durden will not receive a reduced sentence. Felty stated that Durden was on parole when he was caught, which adds time to his sentence. The ankle bracelet worn by the parolee was set for a 7pm curfew. Durden used that opportunity to commit burglaries during daylight hours.
Since the interview was published, the Allen Police Department has received calls from police agencies all over the country asking to use the video for training and for local PSA distribution. The video has had over 38,000 views on YouTube.


Ah, backpacking! And that too backpacking in winters. When I hear this 11-letter word my heart beats faster and mind immediately takes action full on the excitement that I should leave now for a trip. And I believe, the majority of you guys cases are like this.
But before leaving we should not take backpacking lightly and especially in winters.
Because we are heading to a place which will be too far from the home and we don't want to end up buying that same thing which has existed in the home.
We will be focusing on the much-needed things while backpacking in the winters.
We tend to lose energy quickly in winters while we are on trips..The long walking and exploring takes all the energy and sometimes night too. Water also plays a perfect role. But energy drinks are very beneficial here.
Homemade energy drinks and very effective as well as suited according to your needs.
The first thing we all focus, is our warm clothes in winters. Not only packing warm but dressing in the case.,how many of us actually end up dressing warm in winters, that the clothes really sound like warm.
Hardly a few of them and ends up talking we had worn so many layers but why am I still feeling my body cold. It's because of not wearing appropriately.
Also read, things to focus for the first-time backpacker.
Now, shoes. The more we focus on our clothes while backpacking, the less we Pay attention to our shoes and that's really important because of this we will make a strong grip on the ground and if there are snow shoes are damn handy!
When we are talking about things to focus while backpacking in winters then why to ignore backpacks here. Would you like to take a not so good one? No Na.
These backpacks are the bone of travelers where almost anything related to travel can be found and uploaded in a backpack.
Is this thing really existing in today's time? Shockingly Yes. Lol. With the coming of new trends, socks are left alone with the shoes. But don't do this in winters and especially if there is snow.
Keeping your socks dry is the most difficult things in winters and snow comes in between to make you feel cold.
Winter socks are really helpful. Remember.
Thermal Flask keeps water warm. In the cold winters, this will bring relief from the conditions and you must include this in your backpack. Warm water in winters is like looking for water in the hot desert.
I think your bag must be full now.
Don't make it full, then where you will be going to keep your medicines, camera etc.
These are the things which I find most important to consider for winters while backpacking.
Follow me on my social media to know more about me.
Thank you for the comment.Try it and you will love this and it will going to be your lifetime memorable too.
I never had the chance to go backpacking so I will keep these tips in mind for when I get the cgances to go! Hopefully soon!!
Thank you for taking a time out in reading. This means a lot. Hopefully you will be going soon. Happy traveling.
Definitely going to pay attention to this if I ever go backpacking. I'm going on a long weekend to Spain but not sure that counts as Winter haha, although Ryanair make you take the smallest bag ever!
Thank you for reading. Have a happy and blissful journey to spain.
That's amazing. Majority of us actually don't do this so it's good to hear from you. Thank you for reading.
Excellent tips!! I love travel but I have never been backpacking – I do love the thought of going travelling with only what you have in your bag. But as someone who struggles to pack light, I am not sure how well I could manage to fit everything in one bag. Hopefully I will do it one day – there are so many amazing places in this world, why stay in one place?
Absolutely Hayley, why stay in one place when you have so much to explore. Hope you will do backpacking one day and enjoy the experience. Thank you so much for reading and sharing your thoughts with me .
Great tips for sure! While we dont live in an area where it gets overly cold or snowy it's a trip I would love to take the kids on some day as I grew up with snow and feel like they are really missing out in some fun! These tips will be more them helpful when the time comes!
Thank you so much. I also don't leave in a place where it snows but whenever I feel that this is the time I leave for mountains and snow.
This is a kind of fun in winters , wearing thermal base and long boots has its own charm. Thank you so much for reading.


text:
Virat Kohli records 250th appearance: Which Indian captain has played most ODI matches for Men In Blue?
On Sunday, Indian skipper Virat Kohli became the 8th cricketer to play 250 matches for the Men In Blue. Which Indian captain has played most ODI matches for Men In Blue?
Virat Kohli records 250th appearance: Which Indian captain has played most ODI matches for Men In Blue? | &nbspPhoto Credit:&nbspAP
Indian skipper Virat Kohli entered the 250 club on Sunday
The Indian skipper has become the 8th cricketer to play 250 matches for the Men In Blue
Which Indian captain has played most ODI matches for Team India?
Indian skipper Virat Kohli only had to arrive for the coin toss on Sunday to add another feather into his already illustrious cap in white-ball cricket. Leading the Team India in the 2nd One Day International (ODI) against hosts Aaron Finch-led Australia, Indian skipper Kohli recorded his 250th appearances for the two-time World Champions in the 50-over format.
After suffering a heavy defeat at the hands of five-time World Champions in the bilateral series opener, Kohli-led Team India opted to make no changes in the penultimate clash of the three-match rubber between the two cricketing superpowers. Kohli was congratulated by the match broadcasters for recording his 250th ODI appearance following the toss at the famous Sydney Cricket Ground in Australia.
Joining the elite list starring the likes of Sachin Tendulkar, MS Dhoni, Rahul Dravid, Mohammad Azharuddin, Sourav Ganguly, and others, Kohli became the eighth Indian to play as many as 250 matches for the Men In Blue. Master Blaster Tendulkar tops the list of Indians with the most number of matches in the 50-over format. In his iconic career that spanned more than two decades, Tendulkar played 464 ODI matches for the Men In Blue.
Talking about the 250 club in ODIs, legendary Indian all-rounder Yuvraj Singh (269) and ace spinner Anil Kumble (301) have also played more than 250 matches for the Indian national team. Skipper Kohli is behind the likes of Dhoni (200), Azharuddin (174), and Ganguly (147) in the list of Indian players with the most matches as captain.
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For India, legendary wicket-keeper batsman and two-time World Cup winner Dhoni has led the national side in 200 matches - the most by any Indian captain in the history of ODI cricket. Dhoni played 347 matches for Team India in which the Ranchi stalwart recorded 110 wins as captain. Overall, former Australian skipper Ricky Ponting has played the most international matches as captain (230). Ponting is followed by Stephen Fleming (218) and Dhoni (200) in the elite list.


text:
Q: How can I read values from a static config.json file to TypeScript in a Vue file after running build:electron in Vue CLI 3? Good afternoon.
I was wondering whether it is possible to add a config.json file to a Vue CLI 3 project that can be read at runtime, both during development and production.
The config.json file will contain some strings the app can use to change content dynamically, such as the video files that are displayed to a user and the IP address of a printer.
// config.json

{
    "brand": "eat",
    "printerIP": "192.168.0.4"
}

I have attempted to place the file in the assets folder and the public folder. I have tried importing it to the script lang="ts" element of App.vue using both import and require statements. I am using the vue-property-decorator.
// App.vue (<script lang="ts">)

const config = require('../public/config.json');

OR

import config from '../public/config.json';

I have accessed the values both by processing it like an API using axios and simply accessing the variables using, for example, config.brand.
// App.vue (<script lang="ts">)

import axios from 'axios';

@Provide() private brand: string = "";

axios
    .get('.config.json')
    .then(response => {
        this.brand = response.data.brand;
    })

OR

this.brand = config.brand;

Unfortunately, the data is only read at build time and compiled into minified JavaScript. This means the app is not updated even if the user updates the variables in config.json after the app is built. I need to be able to access config.json in the build files, update a value and then have the app read the new value at runtime without the need to build the project again. I was wondering if it is possible to do this.
Any help you can provide will be greatly appreciated.

A: You're right in thinking that you should put runtime configurations under the public/ folder, but don't import them. The import would get resolved during build time and its result would go through webpack. Instead, use fetch to load them via HTTP.
Vue designates the public folder as the place to put static assets that should bypass webpack and simply by copied to dist/. You can access them during runtime with an HTTP request like this:
const getRuntimeConfig = async () => {
  const runtimeConfig = await fetch('/config');
  return await runtimeConfig.json()
}

If you want to use those runtime configurations in multiple Vue components without doing multiple fetches, then do one fetch in the main Javascript file that drives your Vue app (e.g. src/main.js) and share the result via Vue mixins, like this:
  Vue.mixin({
      data() {
        return {
          // Distribute runtime configs into every Vue component
          BRAND: BRAND,
          PRINTER_IP: json.printerIP
        }
      },
    });


text:
Q: how to read a file, store data and then write it I have a text file with a ton of values that I want to convert to meaningful JSON using node.js fs module.
I want to store the first value of every line in an array unless the value is already present.
7000111,-1.31349,36.699959,1004,
7000111,-1.311739,36.698589,1005,
8002311,-1.262245,36.765884,2020,
8002311,-1.261135,36.767544,2021,

So for this case, I'd like to write to a file:
[7000111, 8002311]
Here's what I have so far. It writes [] to the file.
var fs = require('fs');
var through = require('through');
var split = require('split');
var shape_ids = [];

var source = fs.createReadStream('data/shapes.txt');
var target = fs.createWriteStream('./output3.txt');

var tr = through(write, end);

source
    .pipe(split())
    .pipe(tr)

// Function definitions

function write(line){
    var line = line.toString();
    var splitted = line.split(',');

    // if it's not in array
    if (shape_ids.indexOf(splitted[0]) > -1){
        shape_ids.push(splitted[0]);
    }
}

function end(){
    shape_ids = JSON.stringify(shape_ids);
    target.write(shape_ids);
    console.log('data written');
}

The code is using the split and through modules
How do I store values in the array and write the populated array to the file?
== === ====== =================
Update:
This is what I want to do, but it's in Ruby:
shape_ids = []

File.open("data/shapes.txt").readlines.each do |line|
   data = line.split(',')
   shape_id = data.first

   if !shape_ids.include? shape_id
       shape_ids.push(shape_id)
   end
end

puts shape_ids  # array of unique shape_ids

Can I do this in javascript?

A: Unless you are super comfortable with the new Stream API in node, use the event-stream module to accomplish this:
var fs = require('fs');
var es = require('event-stream');

function getIds(src, target, callback) {
  var uniqueIDs = [];
  es.pipeline(
    fs.createReadStream(src),
    es.split(),
    es.map(function (line, done) {
      var id = line.split(',').shift();
      if (uniqueIDs.indexOf(id) > -1) return done();
      uniqueIDs.push(id);
      done(null);
    }),
    es.wait(function (err, text) {
      // Here we create our JSON — keep in mind that valid JSON starts
      // as an object, not an array
      var data = JSON.stringify({ ids: uniqueIDs});
      fs.writeFile(target, data, function (err) {
        if ('function' == typeof callback) callback(err);
      });
    })
  );
}

getIds('./values.txt', './output.json');

Unfortunately there is no "easy" way to keep this as a pure stream flow so you have to "wait" until the data is done filtering before turning into a JSON string. Hope that helps!