Grandmaster Chen Zhenglei 2018 Symposium

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2018Symposium

 

Fifth Annual Symposium at Chenjiagou June 27th to July 4. This year the theme color is red symbolizing vigor and enthusiasm and the keyword is ‘benevolence’, specifically “Realizing the Tai Chi Chuan Ideal with the heart of a benevolent warrior”.

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Lowering the Bar (continued)

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I e-asked the esteemed Tom Bisio IF it was not top-secret would volume 7 of his Nei Gong series will have any exercises for the bottoms of the feet. Tom Bisio said no volume 7 planned and no exercises for ankles or feet. However, he encouraged me to publish.

In terms of tai chi bar, I am probably a poor test subject. I get irregular or inconsistent results – partly rolling and partly sliding of the bar, so I figured that was me doing something wrong with the two pressures:

1. there’s the vertical (downward) vector of some weight on the foot and
2. the more or less horizontal pressure trying to move parallel to the ground.

There are, as readers have likely guessed, two versions of the stationary bar. In one the bar can spin parallel to the ground somewhat similar to toilet paper. In the other version the bar does not move at all. No one (not one person) thinks either of these is satisfactory. The primary complaints have been (1) not enough pressure on the heel; (2) skips over the section between about the middle of the foot to just past the cuneiform bones (3) misses the distal metatarsals.

I have asked about the so-called porcupine balls. To needle Charles Tauber, so as to speak, I said I had nothing against the famed Canadian super-rodent (Erethizon dorsatum – below right), but the balls more closely resemble a hedgehog (below left). In either case very few people think the gizmos do any good as they are too flexible and too mobile so there is nothing deeper than tickling the skin. Charles was none too enthused about the idea of rolling the bar guided by grooves. So I suppose we will look into rolling a smooth bar (like a bang) inside a box.

Lowering the Bar (continued)

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I e-wrote to the esteemed Charles Tauber of Toronto “If there is a bang about 6″ long with its raised end ridges rolling in two routed grooves I think, pending your advice, the platform could be something like 12″ long and 10″ wide with the two grooves six inches apart and two inches in from the 12″ edges. I think the grooves could be 11″ long. If not grooves maybesomething like box where a tool like a bang rolls between two walls ”

I mentioned to him that I am not sure if the ridges and grooves are best as v-shapes or square. Likewise, I am not sure about o-rings or just wood. In his reply he favors the two-sided box. I am guessing sufferers are barefoot or have a sock on but not a shoe. The challenge is to massage the foot equally without having the platform move around. I’d be trying to measure downward pressure along the grooves (pr the platform) with sensors.

My take at the moment is that tai chi bar is not very closely related to tai chi ruler. If one wants to say that much of tai chi bang is working on wrists and hands then I would say not much of a resemblance there either. There’s just no leverage applied to the ankle, for example.

I am still not persuaded that the tai chi bar in any of its variants is actually doing much, but some people swear by it, so I am staying the course. Readers may be amused to hear the variants include golf balls and baseballs as well as hard plastic dog bones. One comment I got a lot of was people needing to ‘massage’ their feet in the morning. I am not sure what was going on with sleeping but the claims are they were not really able to walk if they got straight up. So, the regimen is wake up, sit up on the edge of the bed, move one foot at a time over the tai chi bar or equivalent, then stand with support and move one foot at a time over the tai chi bar. Then they are ready to take on the day.

I was somewhat surprised to hear that this was not just seniors but people in their late 40s and even some teenagers. They are also reporting what is supposed to be positive flexing of the knees. If these folks had been serious cyclists or a marathon runners I could understand the impact of years of training in feet and knees. But everyone (so far) is very close to typical.

Lowering the Bar

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In some cases within the cerebral palsy and arthrogryposis spectra there’s an associated arthritis-like condition that was thought to be focused on the fingers, wrists and forearms. So far, not much reporting of hand, elbow or shoulder problems. The symptoms range from loss of flexion to paroxyms of pain (like the wrists are on fire) to a constant dull ache. When I asked almost everyone said, “Wow! Now that you mention it, there are foot problems, but they get overwhelmed by arm problems.” I appreciate most people write, eat, wash, open doors and do sign language with their hands. In any case, the genetics and biochemistry can accurately be described as ‘poorly understood’ .

I am not close to persuaded that the six so-called tai chi tools really originated in either Chen or Yang style Tai Chi Chuan. But no matter – we have what we have. The one tool that stands out as really different is the tai chi bar (rightmost below). As far as I can tell, the object with the Tai Chi Bar is to mechanically massage the bottoms of the feet one sole at a time. This is something of a challenge to any meridian-based theory as we are really only talking about two acupuncture points on the sole of the foot – kidney 2 and the the critical bubbling well aka kidney 1. The other five leg meridians – bladder, gall bladder, stomach, spleen and liver – concentrate on the top of the foot.

Tai-Chi-stick-Tai-Chi-rulers-stick-sandalwood-rosewood-green-Ebony-Wood-Taiji-bar

Bravery and Heroism

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In a much earlier blog entry (https://silverwolfwushu.wordpress.com/2016/04/25/from-great-britain/) in the context of J.R.R. Tolkien’s The Lord of the Rings I wrote

“It is very tempting 75-odd years later to draw a correspondence with England (=Gondor) and especially London (=Minas Tirith) going through the Battle of Britain (Churchill’s speech June 18 1940; actual combat July 10 to October 31) and the Blitz (dates depend on who is writing the history – perhaps September 7 to May 31 1941) and waiting for help from America (=Rohan). As far as I am aware, no one ever surveyed American politicians and asked if the failure to help the British had, in retrospect, any justification. Any. Any at all.”

Multiple readers recently asked if I considered American politicians opposed to President Roosevelt to be traitors, cowards or just really very unintelligent. From the correspondence of  Hans Thomsen, the charge d’affaires at the German Embassy in Washington DC, and other German diplomats it is clear that there was a large-scale German effort to influence American politics with the objective being to keep the United States out of the war by giving money to American politicians especially in 1940. The first part of my reply was that since 1938 American politicians were required to document where foreign contributions came from. This legal requirement was easily circumvented by both recipients and contributors. So technically, no treason. It is difficult to say whether or not the correspondence of Hans Thomsen was intercepted and de-crypted in 1940. This seems very unlikely as publication of this information at that time would have been electrifying. Rather, it seems that the correspondence materials were confiscated sometime after the declaration of war and not translated immediately.

 

Wrist exercises (continued)

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The second exercise starts with the hands being held in front at chest height but with palms up. The hand scissor together so they are on the centerline with (for example) the left hand over the right so that the right palm is in contact with the back of the left hand. The right thumb goes just below and between the knuckles for the little and ring fingers. Again, the right index finger does nothing. The other three fingers of the right hand hook around the far edge of the wrist (would be the medial part of the wrist normally but the hand is rotated so the medial edge is on the outside). Now the right thumb pushes the left hand so the left hand’s fingers are now pointed at your face. There is tension on the wrist. You then extend the hands outward to stretch the wrist. In both exercises it was stressed that both wrists are being worked.
WristExercisePhoto02Outward
A link to a short video

Wrist exercises (continued)

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Starting with the hand held out palm down at chest height one exercise was to rotate one hand 90 degrees in the vertical plane so the thumb is down (lower) and the little finger is up (higher). The palm is perpendicular to the floor and the fingertips are parallel to the floor. At the same time the other hand rotates in parallel so the thumb is up higher) and the little finger is down (lower) with the palm perpendicular to the floor and the fingertips parallel to the floor. This leaves you with both palms facing the same way. Let’s say you rotated the hand clockwise so the left palm faces out and right palm faces in. The hands move inward toward your centerline and the right palm contacts the top of the left hand. The right thumb crooks over the abductor muscles (“knife edge”) of the left hand. The right index finger doesn’t really do much. The other three fingers of the right hand hook around the left index finger. Now you gently rotate the hands about 30 degrees vertically upward. There should be some tension on the distal knuckles of the left hand (for little and ring fingers) and near the pisiform bone in the wrist. Then you slowly bring the the wrists to touch your breastbone. Repeat for the other wrist.
WristExercisePhoto01Inward

Wrist exercises

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For those with challenges in the cerebral palsy and arthrogryposis spectra there are often losses of flexion in the fingers, hands, wrists and forearms. The accompanying sensations range from an unpleasant tingling to something described as ‘burning arthritis’. So we do a fair amount of exercises designed to maintain if not increase flexibility. Some of these exercises involve wooden ‘tools’ (as opposed to weapons) like the tai chi bang and tai chi ruler. I prefer to pass along the history when I can – that is is easier said than done with the tai chi tools. More about them, including the rarely seen tai chi bar, in the future.
We also do several wrist exercises during warm-ups. I was somewhat shocked to discover that I had no idea where two particular exercises had come from. I had learned them in the early 1970s in Palo Alto California but it was unclear what art they were from. Upon asking around in my own martial arts e-grapevine, a fair number of people said the movements were familiar, and many mentioned that they had learned them in the 1970s or 1980s. I was cheered to hear that some still practiced the particular movements. But no one had a firm opinion where the exercises came from, what art might have originally developed them, who might have taught them or even when. 

No one recalls the esteemed Professor Sig Kufferath (1911-1999; leftmost image below) teaching or doing the exercises, so there is some doubt that the exercises come from Danzan Ryu. Unfortunately, no one could point to an authentic written list of warm-up exercises from Professor Okazaki’s (1890-1951; rightmost image below) classes in Hawaii in the 1930s or 1940s either. There has been some speculation that the exercises were brought from Japan to Hawaii in the 1930s by two Kodokan jushodans who visited Hawaii to teach for extended periods. There are difficulties with the timing if one wants to claim the exercises come from aikido.

 

Possible Progress against Huntington’s Disease (continued)

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HuntingtonsSAITO

Mutations in the HTT gene cause Huntington disease. The HTT gene provides instructions for making a protein called huntingtin. Although the exact function of this protein is unknown, it appears to play an important role in nerve cells (neurons) in the brain. The HTT mutation that causes Huntington disease involves a DNA segment known as a CAG trinucleotide repeat. This segment is made up of a series of three DNA building blocks (cytosine, adenine, and guanine) that appear multiple times in a row. Normally, the CAG segment is repeated 10 to 35 times within the gene. In people with Huntington disease, the CAG segment is repeated 36 to more than 120 times. People with 36 to 39 CAG repeats may or may not develop the signs and symptoms of Huntington disease, while people with 40 or more repeats almost always develop the disorder. An increase in the size of the CAG segment leads to the production of an abnormally long version of the huntingtin protein. The elongated protein is cut into smaller, toxic fragments that bind together and accumulate in neurons, disrupting the normal functions of these cells. The dysfunction and eventual death of neurons in certain areas of the brain underlie the signs and symptoms of Huntington disease.

As the altered HTT gene is passed from one generation to the next, the size of the CAG trinucleotide repeat often increases in size. A larger number of repeats is usually associated with an earlier onset of signs and symptoms. This phenomenon is called anticipation. People with the adult-onset form of Huntington disease typically have 40 to 50 CAG repeats in the HTT gene, while people with the juvenile form of the disorder tend to have more than 60 CAG repeats.

Of the four described Huntington disease-like (HDL) syndromes, HDL4 appears to be the most common. HDL2 is the second most common and occurs almost exclusively in people of African heritage (especially black South Africans). HDL1 has been reported in only one family. HDL3 has been found in two families, both of which were from Saudi Arabia.

In about one percent of people with the characteristic features of Huntington disease no mutation in the HD gene has been identified. However, mutations in the PRNP, JPH3, and TBP genes have been found to cause the signs and symptoms in some of these individuals. HDL1 is caused by mutations in the PRNP gene, while HDL2 results from mutations in JPH3. Mutations in the TBP gene are responsible for HDL4
(also known as spinocerebellar ataxia type 17). The genetic cause of HDL3 is unknown.

One region of the JPH3 gene contains a CAG/CTG trinucleotide repeat.  Normally, the CAG/CTG segment is repeated 6 to 28 times within the gene.  People with HDL2 have 44 to 59 CAG/CTG repeats. People with 29 to about 43 CAG/CTG repeats may or may not develop the signs and symptoms of HDL2.

Normally, the CAG/CAA segment is repeated 25 to 42 times within the TBP gene. People with HDL4 have 43 to 66 CAG/CAA repeats. People with 43 to 48 CAG/CAA repeats may or may not have signs and symptoms, while people with 49 or more repeats almost always develop the disorder.

The PRNP mutations associated with HDL1 involve a segment of DNA called an octapeptide repeat. This segment provides instructions for making eight protein building blocks (amino acids) that are linked to form a protein fragment called a peptide. The octapeptide repeat is normally repeated five times in the PRNP gene. In people with HDL1, this segment is repeated eleven or thirteen times. An increase in the size
of the octapeptide repeat leads to the production of an abnormally long version of PrP. It is unclear how the abnormal protein damages and ultimately destroys neurons, leading to the characteristic features of HDL1.

 

 

Possible Progress against Huntington’s Disease

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It was estimated that about 10,000 people in Great Britain and 65,000 in the United States have Huntington’s Disease (formerly Huntington’s chorea).  There are currently two major groups of symptoms:

1.   adult-onset ( the most common) typically manifests in a person’s 30s or 40s. Challenges in the cognitive areas can include irritability, depression, small involuntary movements, poor coordination, and trouble learning new information or making decisions. The chorea refers to involuntary jerking or twitching movements. These worsen and make walking, speaking, and swallowing difficult.

2. juvenile-onset manifests in childhood or adolescence. Additional challenges include slow movements, clumsiness, frequent falling, rigidity, slurred speech, and drooling. Seizures occur in one third to one half of children with this condition. This variety tends to progress more quickly than adult-onset.

An early understanding of Huntington’s Disease was greatly hampered by the work of Charles Benedict Davenport (June 1, 1866 – February 18, 1944), Elizabeth Muncey, a federal Eugenics Record Office researcher, and the imaginative P. R. Vessie.

The Woman Who Walked into the Sea: Huntington’s and the Making of a Genetic Disease by Alice Wexler (2008 Yale University Press) is worth a read.

An exciting discovery was made after almost twenty years of studying people in two villages in Venezuela. A gene called HTT on chromosome 4 on the p16.3 region had a variable number of nucleotide repeats. The full explanation of what the Huntington protein does exactly still needs work.

Prof Sarah Tabrizi, director of University College London’s Huntington’s Disease Centre who led the phase 1 trial of a drug called Ionis-HTTRx, explained that the interception and destruction of a messenger molecule prevents  the harmful protein from being made. We’ll see what the actual paper reads like and whether the drug scales up safely.