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I am given the news that a consultant paid by Centro has said at the public enquiry into transport that Electroliners (aka Trolley Coaches, aka Trolley buses) are not cost effective.


This, of course, not news. News would be when a consultant paid by Centro said something that centro did not agree with. If someone is paid to write a report they generally write what they are asked to write. The payer of the piper may wave around the report saying "this report agrees with me", but that is generally meaningless.


The other substantial issue that arose at the Cabinet Meeting was the PFI scheme into roads. The PFI scheme is essentially getting the roads improved on Hire Purchase. The headlines look quite good. The City Council gets a "PFI credit" of £379 Million (over 25 years). Indeed it might be good for the city. However, the city loses £175 Million of Local Transport Plan funding and also has to commit to paying out around £50 million a year (index linked) to a private contractor. The figures for this have not been checked. £50 Million a year is about a fifth of the council tax revenues. The problem is that the whole story has not yet been told so it has not been checked. Hence the argument about scrutiny.


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Its the long genes that stop working

People who read my blog will be aware that I have for some time argued that most (if not all) diseases of aging are caused by cells not being able to produce enough of the right proteins. What happens is that certain genes stop functioning because of a metabolic imbalance. I was, however, mystified as to why it was always particular genes that stopped working. Recently, however, there have been three papers produced: Aging is associated with a systemic length-associated transcriptome imbalance Age- or lifestyle-induced accumulation of genotoxicity is associated with a generalized shutdown of long gene transcription and Gene Size Matters: An Analysis of Gene Length in the Human Genome From these it is obvious to see that the genes that stop working are the longer ones. To me it is therefore obvious that if there is a shortage of nuclear Acetyl-CoA then it would mean that the probability of longer Genes being transcribed would be reduced to a greater extent than shorter ones.