oddments

the way the spark plug lead on many mowers is routed, that is, directly touching metal is problematic and the heat of fins eventually damages any cable directly touching it, also providing an earth to the leakage path !

spark plug leads should be clear of any metal, i cut an oversize hole in the cover and suspended the cable through the center with a bit of plastic cut from the wall of a clear plastic bottle and glued in with a contact adhesive !

PET (recycle number 1) seems to be ok for this (comparative dielectric strengths, table 2/3 the way down the page)

i always keep my head well clear of the flywheel and armature when mower is going to minimise magnetic fields damaging the DNA in the brain !

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this mower has a plastic bodied carb (no. 795477) and the warping of the plastic body is an issue, making diaphragm sealing difficult !

the symptom of this is an extremely rich mixture and the plug gets very sooty within minutes and has to be cleaned using P240 W&D sandpaper

also the jet filter wants to be hard up against the intake to restrict the flow into the jet as much as possible as it tends to run rich !

a possibility with the jet is to heat the jet end and squeeze to narrow the orifice?

the problem area is the locus between several chambers and one small valve hole where the distance between them is about 3mm across the flat aluminium so sealing across this is apparently problematic !

i sanded the small valve hole in this area on the plastic with P240 wet and dry (but using dry !) and also the other small valve hole in the aluminium and i think that's helped !

why sanding the small valve holes might have worked is dimpling increases the length of surface the petrol has to move over to escape compared to mirror flat!

i also scribed with parallel lines the locus separation areas on top of sanding, maybe the scribing is not necessary? and will give a light sand with P240 when i next have to pull it apart? or just leave the scribe mark as seems to be working?

i had filed the plastic body previously as flat as i could tell ( a mistake?)

i use the loctite no. 3 non-hardening sealant in a "medium thin" coat on the flat aluminium tank surface in the locus problem area and a dab across the other side to "stick" the diaphragm so it stays in position during futher assembly !

the #3 should be well shaken before using as it can possibly separate a bit if left standing for months and also allowed to air dry for 5 minutes when applied so it becomes tacky !

cotton buds seem clean out any #3 fallen into wells or chambers !

permatex have a similar product to loctite!

i did not coat the diaphragm at all !

i then gently tightened it all up taking care not to over torque

this seems to have worked , but i store the mower with the tank empty, either run out or siphoned and press the red primer knob a couple of times so that theres no petrol left in the carb to possibly revert the loctite no. 3 !

silicon is no good, it just becomes like jelly with the petrol !

2nd jan 2012, the diaphragm sealant only lasts so long, (boiling it seems to give some recovery !) so what seems better is to use an older paper gasket to double up the paper gaskets and replace the nitrile diaphragm quite frequently.

12th june 2013, only use one cardboard gasket and instead of another use an old diaphragm (with the actual diaphram part cut out not to interfere with the real diaphragm action) between the one cardboard gasket and the plastic carb body !

the width of the cardboard gasket varies from .45 to .55mm and the diaphragm is .2mm so the addition of the extra diaphragm is significant !

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RHYME AS A NON VERBAL THERAPY

scott adams who does the dilbert cartoons is, shall we say, on autistic spectrum and regressing in a major way as he gets older !

anyway he became partly non verbal and its interesting to read how he worked around it and i suspect many nonverbal kids are better approached to speaking by rhyme and singing

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“ Good News Day

As regular readers of my blog know, I lost my voice about 18 months ago. Permanently. It's something exotic called Spasmodic Dysphonia. Essentially a part of the brain that controls speech just shuts down in some people, usually after you strain your voice during a bout with allergies (in my case) or some other sort of normal laryngitis. It happens to people in my age bracket.

I asked my doctor – a specialist for this condition – how many people have ever gotten better. Answer: zero. While there's no cure, painful Botox injections through the front of the neck and into the vocal cords can stop the spasms for a few months. That weakens the muscles that otherwise spasm, but your voice is breathy and weak.

The weirdest part of this phenomenon is that speech is processed in different parts of the brain depending on the context. So people with this problem can often sing but they can't talk. In my case I could do my normal professional speaking to large crowds but I could barely whisper and grunt off stage. And most people with this condition report they have the most trouble talking on the telephone or when there is background noise. I can speak normally alone, but not around others. That makes it sound like a social anxiety problem, but it's really just a different context, because I could easily sing to those same people.

I stopped getting the Botox shots because although they allowed me to talk for a few weeks, my voice was too weak for public speaking. So at least until the fall speaking season ended, I chose to maximize my onstage voice at the expense of being able to speak in person.

My family and friends have been great. They read my lips as best they can. They lean in to hear the whispers. They guess. They put up with my six tries to say one word. And my personality is completely altered. My normal wittiness becomes slow and deliberate. And often, when it takes effort to speak a word intelligibly, the wrong word comes out because too much of my focus is on the effort of talking instead of the thinking of what to say. So a lot of the things that came out of my mouth frankly made no sense.

To state the obvious, much of life's pleasure is diminished when you can't speak. It has been tough.

But have I mentioned I'm an optimist?

Just because no one has ever gotten better from Spasmodic Dysphonia before doesn't mean I can't be the first. So every day for months and months I tried new tricks to regain my voice. I visualized speaking correctly and repeatedly told myself I could (affirmations). I used self hypnosis. I used voice therapy exercises. I spoke in higher pitches, or changing pitches. I observed when my voice worked best and when it was worst and looked for patterns. I tried speaking in foreign accents. I tried "singing" some words that were especially hard.

My theory was that the part of my brain responsible for normal speech was still intact, but for some reason had become disconnected from the neural pathways to my vocal cords. (That's consistent with any expert's best guess of what's happening with Spasmodic Dysphonia. It's somewhat mysterious.) And so I reasoned that there was some way to remap that connection. All I needed to do was find the type of speaking or context most similar – but still different enough – from normal speech that still worked. Once I could speak in that slightly different context, I would continue to close the gap between the different-context speech and normal speech until my neural pathways remapped. Well, that was my theory. But I'm no brain surgeon.

The day before yesterday, while helping on a homework assignment, I noticed I could speak perfectly in rhyme. Rhyme was a context I hadn't considered. A poem isn't singing and it isn't regular talking. But for some reason the context is just different enough from normal speech that my brain handled it fine.

Jack be nimble, Jack be quick.
Jack jumped over the candlestick.

I repeated it dozens of times, partly because I could. It was effortless, even though it was similar to regular speech. I enjoyed repeating it, hearing the sound of my own voice working almost flawlessly. I longed for that sound, and the memory of normal speech. Perhaps the rhyme took me back to my own childhood too. Or maybe it's just plain catchy. I enjoyed repeating it more than I should have. Then something happened.

My brain remapped.

My speech returned.

Not 100%, but close, like a car starting up on a cold winter night. And so I talked that night. A lot. And all the next day. A few times I felt my voice slipping away, so I repeated the nursery rhyme and tuned it back in. By the following night my voice was almost completely normal.

When I say my brain remapped, that's the best description I have. During the worst of my voice problems, I would know in advance that I couldn't get a word out. It was if I could feel the lack of connection between my brain and my vocal cords. But suddenly, yesterday, I felt the connection again. It wasn't just being able to speak, it was KNOWING how. The knowing returned.

I still don't know if this is permanent. But I do know that for one day I got to speak normally. And this is one of the happiest days of my life. ”

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DINOSAURS AND WEIGHT LOSS

there's a bit of contention as to wether dinosaurs are birds, or birds and dinosaurs shared a common ancestor, i think the evidence is pointing towards sharing a common ancestor

to sequence 68 million year old dna is just so astounding

dinosaurs, birds and lizards don't have any brown fat so they have trouble keeping warm, its why birds migrate and probably a big factor in the extinction of dinosaurs

white fat is for storage and brown fat is what is burnt for energy, i would assume overweight people are deficient in nutrients that are needed to convert white to brown fat or may even have an altered genetic expression favouring white over brown fat

brown fat helps newborn and adult mammals maintain their body temperature by burning fat, which converts into heat. The protein UCP1 (Uncoupling Protein 1) has a key role in this energy conversion, which takes place in the cell mitochondria

interestingly pigs have lost this protein study

"Piglets appear to lack brown adipose tissue, a specific type of fat that is essential for nonshivering thermogenesis in mammals, and they rely on shivering as the main mechanism for thermoregulation. Here we provide a genetic explanation for the poor thermoregulation in pigs as we demonstrate that the gene for uncoupling protein 1 (UCP1) was disrupted in the pig lineage. UCP1 is exclusively expressed in brown adipose tissue and plays a crucial role for thermogenesis by uncoupling oxidative phosphorylation."

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THE ANGIOTENSIN CONVERTING ENZYME AND WEIGHT LOSS

i must have low levels of the angiotensin converting enzyme

can't put on fat if i tried, have lowish blood pressure and sure burn through sugar

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Australian scientists believe they may have discovered how to help people lose weight without cutting back on food.

Researchers in Melbourne found that by manipulating fat cells in mice they were able to speed up metabolism.

After removing a particular enzyme, scientists found the mice were able to eat the same amount as others but burn more calories and gain less weight.

The breakthrough could pave the way for fat-burning drugs and also help to combat diabetes.

The research found that mice in which the angiotensin converting enzyme (ACE) had been removed were, on average, 20% lighter than normal mice and had up to 60% less body fat.

Because of their faster metabolisms, it also appeared they had less chance of developing diabetes because they processed sugar more quickly.

Drugs which impair the action of ACE in humans already exist, and are used to combat high blood pressure.

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WAIST TO HEIGHT RATIO PREDICTIVE OF TYPES 2 DIABETES FOR WOMEN

i'm in the clear, i'm not a woman and i don't have a waist ;o)

its real interesting actually

what they are saying is that since the number of abdominal fat cells remains constant after adolescence

then more girth on the waist is due to those fat cells getting bigger

this increase in the size of fat cells is the real signaller for increased type 2 diabetes risk (insulin resistance)

its odd, i eat huge amounts of fat yet have practially no fat on me at all and i have always been pretty much this way

the latest research is showing that it's the increase in fat cell size thats very problematic so increasing abdominal fat given that the number of cells stay relatively constant is a very good marker of increasing cell size which is why "pear shaped" is such telling symptom of metabolic syndrome

com'n fatties, fess up

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Size of fat cells and waist size predict type 2 diabetes in women (october 2009)

When it comes to assessing risk for type 2 diabetes, not only do waistlines matter to women, but so does the size of their fat cells. This new discovery helps explain why some women of normal weight develop type 2 diabetes, despite not having any known risk factors.

“Increased knowledge of the link between enlarged fat cells and the development of type 2 diabetes may give rise to new preventive and therapeutic alternatives. Our research also identifies the ratio waist-to-height, waist circumference divided by body height, as a simple tool that can be used to identify women at risk of developing type 2 diabetes.”

The data for this discovery were obtained as part of the "Prospective Study of Women in Gothenburg," performed in Sweden and started in 1968 . For this study, a team of Swedish researchers invited women to free health examinations over the course of 25 years. In 1974-1975, scientists collected abdominal fat biopsies from some of the women and tracked who developed type 2 diabetes. They found that the number of abdominal fat cells remained relatively constant in women after adolescence, but the size of fat cells could change considerably throughout life and were larger in women with type 2 diabetes. In addition, they found that waist-to-height ratio may also be a good indicator of diabetes risk.

According to the U.S. Centers for Disease Control and Prevention, type 2 diabetes may account for 90 to 95 percent of all diagnosed cases of diabetes. The disease begins as insulin resistance, and as the need for insulin rises, the pancreas gradually loses its ability to produce insulin. Type 2 diabetes often is associated with older age, but is increasingly being diagnosed in children. Obesity, family history of diabetes, history of gestational diabetes, impaired glucose metabolism, physical inactivity, and race/ethnicity also play a role in whether or not someone develops the disease. In particular, African Americans, Hispanic/Latino Americans, American Indians/Native Americans, and some Asian Americans and Native Hawaiians or Other Pacific Islanders are at high risk for type 2 diabetes.

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BODY WEIGHT INFLUENCED BY THOUSANDS OF GENES

obesity is a condition of trace mineral malnutrition, biofilm toxins and a lack of skin vitamin D which is addressed by the compendium™ and BCD™

its really a symptom and can't be addressed directly, as you can see from the study below estimating 25% of the bodies genes have an impact on weight

thats basically why all the weight loss programs are fools gold, no shortage of those ;o)

the compendium and BCD do give an excellent and optimal body shape, the roots of the biofilm carbohydrate diet go back to the early greek games and the very first olympics in 776 BC as an athletes diet

weight problems should be judged by looking at the body shape and bone structure, overweight should always be judged visually like this and never be checked by weight

skinny is the bodies response to reducing the metabolic load, so you have to look at the reason why and work from causes and not attempt to build up weight or muscle mass directly as this just increases the metabolic load which the body couldn't cope with in the first place, muscle is especially very metabolically expensive as you may notice with all the brain dead and joint damaged bodybuilders

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PHILADELPHIA (January 14, 2008) – Reporting in the online journal BMC Genetics, researchers from the Monell Center have for the first time attempted to count the number of genes that contribute to obesity and body weight.

The findings suggest that over 6,000 genes – about 25 percent of the genome – help determine an individual's body weight.

"Reports describing the discovery of a new `obesity gene' have become common in the scientific literature and also the popular press," notes Monell behavioral geneticist Michael G. Tordoff, PhD, an author on the study.

"Our results suggest that each newly discovered gene is just one of the many thousands that influence body weight, so a quick fix to the obesity problem is unlikely."

To obtain an estimate of how many genes contribute to body weight, the Monell researchers surveyed the Jackson Laboratory Mouse Genome Database for information on body weights of knockout mouse strains.

Knockout mice have had a specific gene inactivated, or "knocked out." By studying how the knockout mice differ from normal mice, researchers obtain information about that gene's function and how it might contribute to disease. Mice can provide valuable information on human disease because they share many genes with humans.

The knockout approach is so useful that the inventors of the technology were awarded the 2007 Nobel Prize in Medicine. Knockout mice are now standard tools in all mouse models of behavior and disease.

In 60% of strains, knocking out a gene produces mice that are nonviable; that is, the mouse cannot survive without the knocked out gene.

The Monell survey revealed that body weight was altered in over a third of the viable knockout stains; 31 percent weighed less than controls (indicating that the missing genes contribute to heavier body weight), while another 3 percent weighed more (contributing to lighter weight).

Extrapolating from the total number of genes in the mouse genome, this implies that over 6,000 genes could potentially contribute to the body weight of a mouse.

Tordoff comments, "It is interesting that there are 10 times more genes that increase body weight than decrease it, which might help explain why it is easier to gain weight than lose it."

Because body weight plays a role in many diseases, including hypertension, diabetes, and heart disease, the implications of the findings extend beyond studies of obesity and body weight. Gene knockouts reported to affect these diseases and others could potentially be due to a general effect to lower body weight.

The findings also hold clinical relevance, according to lead author Danielle R. Reed, PhD, a Monell geneticist.

“ Clinicians and other professionals concerned with the development of personalized medicine need to expand their ideas of genetics to recognize that many genes act together to determine disease susceptibility. ”

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THE COMPENDIUM AND THE BCD FOR WEIGHT LOSS

obesity is a condition of malnutrition as well as being partly genetic

the genetic side makes it not very tractable if you (the obese!) remain in your present dietary and nutritional space, especially vitamin D deficiency

if you want to get out you have to traverse to that super metabolic space your body and biochemistry will inhabit on the full compendium which includes adequate skin vitamin D

the full compendium and BCD can give a superbly shaped body, interestingly, the SCD and BCD have their origins going back to the original greek olympics as an athletes diet