Acid Bit

By Russ Miller

 The more we learn about human DNA the more apparent it becomes that Darwinists are blowing hot air with their claims that some apelike creature lurks in man’s ancestral closet.

Scientists who study such things say that human DNA molecules EACH contain enough hereditary data to fill a 500,000-page book. This data is translated by enzymes, all of which are encoded to protect against mutational defects. Both the genetic data and the enzymes that decode the information had to be there from the very start.

For this reason, gradual evolution makes no sense at all.

Still, Darwinists teach that mankind evolved over long periods of time from some sort of an unknown apelike ancestor, often claiming that Human DNA is 98% the same as the DNA found in a chimpanzee.

Let’s examine the truth and determine if this claim has any integrity or validity.

As far as the integrity of this claim, it was based on only about 1% of the total genome. The 1% that was compared was the part controlling body design. Since people and apes have two arms and two legs, the fact that this portion of their DNA strands is rather similar was to be expected. To promote the claim that this proves we are 98% the same in our overall DNA as a chimpanzee is plainly dishonest and highly misleading.

So what about the viability of the claim that people evolved from apes?

Nature magazine has reported that as real science gets into the genome the wider the gap in genetic similarities becomes between man and ape. In fact, scientific studies reveal that there is at least a 7.7% difference between ape DNA and human DNA.

How big of a difference is that?

Well, consider that you contain about three billion base pairs of genetic information in every single one of your DNA-carrying cells throughout your entire body (Do you really think that this kind of complex data formed without any intelligence behind it?).

Just a 7.7% difference between a human’s genetic data and the gene pool found in a chimpanzee would mathematically require 231,000,000 beneficial and new genetic-information-adding mutations to take place in order to change a chimp into a human.

But not even ONE is possible.

Keep these two facts in mind:

First, science knows of no way for nature to add appreciable amounts of new and beneficial genetic information to an existing gene pool.

Second, so many mutations are fatal that there is no mathematical possibility of stringing together 231 million in a row without exterminating the potential evolving individual.

So why don’t Darwinists stop promoting misleading information and just bring out the real evidence that we evolved from a single-celled creature?

Because there is not any real evidence to back up their claims.

Russ Miller is author of The GENESIS Report Series. Register at http://www.new-earth-thought.com to receive FREE his 50 Facts vs. Darwinism e-mail series.

So You Think You Can Destroy Evidence With Fire
By Rachel Yoshida

 Criminals will go to almost any lengths to cover their tracks when they commit a crime that will send them to jail. Starting a fire deliberately will send them to jail also, but sometimes the act they committed will be worse than a fire. People have been using fire to destroy evidence and cover up crimes for hundreds of years or longer and probably at the top of the list is murder.

These days some criminals have learned the hard way that using fire to cover up a crime might not be as easy as it used to be. There have been so many new techniques developed to bring the truth straight out of the ashes. It should make any law breaker afraid of relying on a fire to get away with anything.

In the first place, a criminal will sometimes use some sort of accelerant to start the fire and it is easy for fire investigators to spot this today. They might also use a lighter or matches, but when they use accelerants to start the fire it is a more reliable way to ensure the fire will burn longer and hotter than using other methods. Trained dogs can be used to sniff out accelerants like gasoline, charcoal starter, or other flammable liquids that a criminal might use.

Murderers make the mistake of thinking that a fire can destroy a human body to the point that it can not be identified, but dental records or any trace of DNA can still be use for identification. A murderer might also think that a fire will cover up the cause of a death, but that is not necessarily true either. If there is any usable remains left, many times a coroner will be able to find the cause of death especially if a poison or sever trauma to the body was used.

So actually, when it comes to using fires to cover up crimes today, there is a very good possibility that someone will still be caught and prosecuted for their crime. It is no sure bet that a fire will destroy all evidence that can the guilt of someone or the actual facts of a case. If someone wants to get away with something, they might want to look for an alternative to setting fire to the scene because it is no where near as reliable as it once was.

Rachel Yoshida is a writer of many topics, visit some of her sites, like

Water Damage Restoration and Chicago Water Damage Restoration.

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Will Transcranial Magnetic Stimulation Get FDA Approval?
By Robert Webb

 Neuronetics had tried last year (Jan 2007) to get FDA approval for its transcranial magnetic stimulation (TMS) device, but failed spectacularly. Transcanial magnetic stimulation is a way of non-invasively stimulating the brain with electromagnetism. So what the heck happened with the trial? Neuronetics showed the results of a clinical trial of TMS for major depression to a board of FDA advisors.

The primary efficacy outcome in the clinical trial was the reduction in the Montgomery-Asberg Depression Rating Scale (MADRS) symptom score after 6 weeks. Secondary outcomes included changes in the 17- and 24-item Hamilton Depression Rating Scale (HAMD) (pdf). In the trial, the mean decrease in the MADRS scores was about 5.6 points in the active TMS and around 3.2 points in the sham TMS. Unfortunately for neuronetics, the p-value at the six week mark was .058. A p-value less than .05 is usually that difference between sham and active TMS that is considered statistically significant.

Anything higher than a value of .05 means that the trial technically failed to reach statistical significance. Since the MADRS was the primary outcome measure and it had a p value over .05, this was the statistic that caused the FDA to recommend against approval for the TMS device. The FDA could not get over the fact that the mean score on the MADRS was technically not statistically significant over placebo in the mean change in depression scores for patients. Statisticians argued to the FDA that a p-value of .058 is clinically indistinguishable from a p-value of .05, but that wasn’t good enough for the board evaluating the TMS device.

Looking at the other statistics this specifc trial, the active TMS did reach statistical significance over sham when measured by the secondary outcome symptom scales (HAMD-17 and HAMD-24). So why is it that the TMS device did reach statistical significance on some measures but not others? Well, the MADRS, HAMD-17 and HAMD-24 (pdf) are 3 different scales with completely different rating items.

The TMS is activating a specific area of the brain (the left dorsolateral prefrontal cortex (LDPFC)). Left dorsolateral prefrontal dysfunction (LDPFC) is associated with pseudodepressive symptoms. These type of symptoms include apathy, indifference, anergia, poor concentration and psychomotor retardation. So what likely happened on the neuronetics trial is that specific ratings scales may load more or less heavily on LDPFC dysfunction. The MADRS may not have reached statistical significance because not enough items measured the pseudodepressed type of symptoms associated with LDPFC dysfunction.

This past november (2007), neuronetics had gotten results from a new trial. Surprisingly neuronetics again used the reduction in mean MADRS scores as the primary outcome measure but after 4 weeks instead of 6 weeks. For this new trial, active TMS does show statistically significant improvement over sham TMS with a p-value of .038. Unfortunately there is only a trend for more improvement evident at six weeks with a p-value of .052. The difference between active and sham just missed statistical significance at the six week mark. Both HAMD-17 and HAMD-24 had a reduction in mean scores that was statistically significant for the active treatment over sham (P=0.006 and P=0.012) at four weeks and at six weeks (P=0.005 and P=0.015).

So in this second trial, they at least got clinical efficacy on their primary measure. However that fact that the MADRS mean score didn’t distinguish itself from sham after six weeks is not so good. Will the FDA see past this fact and approve the device? It seems that it will be a close call, but I don’t have confidence that it will be approved. Neuronetics really messed up on both of these trials. If they had looked at the specific rating scale items, they probably could have predicted which rating scale to use as a primary outcome measure.

My guess is that there was a greater reduction in symptoms as measured by the HAMD rating scale because the items load more on LDPFC dysfunction than the MADRS scale. Not to mention that neuronetics used treatment resistant depressed patients in the trial. They are much less likely to respond to treatment than normal patients and make the end results of the trial look, well, depressing.

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