A bit of confusion: astronomy, astrology, and Health Care

This comes from an article entitled, “Did NASA Unearth Life and a Hidden Ocean on Saturn’s Moon Titan?” published at:


NASA announced a few days ago that the Cassini spacecraft had made measurements of changes in Titan’s shape as it orbited Saturn, which they interpreted to mean that a huge underground ocean on the moon was undergoing tidal shifts due to the pull of the planet’s gravity. 

The whole article is worth reading due to its bizarre mix of science and… something. Here are the highlights:

From the article:

“Cassini’s detection of large tides on Titan leads to the almost inescapable conclusion that there is a hidden ocean at depth,” said Luciano Iess, the lead author of the report and a Cassini team member at the Sapienza University of Rome, Italy in a news release issued by NASA.

Donna Stellhorn, an astrologer from somewhere (presumably the Earth), reached the following conclusions:

“From an astrological point of view this discovery signals that we should be asking ourselves is: ‘where do we need to stretch ourselves’ to gain what we want?”


“Saturn in Libra brings us a strong sense of duty and obligation to others whether they be friends or the community at large (hence the passing of the Affordable Care Act),” she said. “But Saturn in Libra can also make us inhibited around others, we want to guard and protect ourselves from potential danger and ridicule.”


Saturn will leave Libra around October 5 and “as he leaves he will take something from each of us; a friendship or relationship may end, your career may shift, or an opportunity may escape you.”

Gotta keep our eyes on those NASA satellites, eh? Never has it been clearer that space data can guide our lives, telling us how to vote and when to end relationships…

Tennis player Andy Roddick states basic principle of (science) communication

When asked about a possible return to next year’s Wimbledon tournement, ousted player Andy Roddick stated:

“If I don’t have a definitive answer in my own mind, it’s going to be tough for me to articulate a definitive answer to you,” he said.


Serena Williams racks up Wimbledon-record 23 aces; Andy Roddick ousted – The DenverPost



Circular definitions

From an early incarnation of the website:


What is Systems Biology?

The emerging area of systems biology is a whole-istic approach to understanding biology.

It aims at system-level understanding of biology, and to understand biological systems as a system.

What was that rule we learned in grade school? When you’re defining a word or term, avoid using the word itself in the definition? (Thanks, Mrs. Thomas!)

“Alien life certain to exist…”

Excerpts from news stories about life on a newly discovered exoplanet:

Sept. 30, 2010

Alien life certain to exist on Earth-like plant, scientists say

The chances of alien life existing on a newly-discovered Earth-like planet are 100 per cent, an astronomer has claimed.


Gliese 581g was discovered orbiting a nearby star at a distance that places it squarely in the “habitable zone” where liquid could exist on its surface…

It is as yet unknown whether water does exist on the planet or what kind of atmosphere it has. But because conditions are ideal for liquid, which is always a precursor for life on Earth, Prof. Vogt believes that life will undoubtedly have begun there.

“Personally, given the ubiquity and propensity of life to flourish wherever it can, I would say, my own personal feeling is that the chances of life on this planet are 100 percent,” he said during a press briefing. “I have almost no doubt about it.”


Nov. 1, 2010

Bye bye to a Lovely Planet

The planet Gliese 581g may be a chimera.

A new analysis by astronomer Michel Mayor and his Swiss team suggests that Gliese 581g is… a planet conjured into existence by other researchers’ fautly interpretations of noisy data.

Where touch meets hearing

Touch sensitivity is hereditary and linked to genetic mechanisms that support hearing

Vision and hearing are so crucial to our daily lives that any impairments usually become obvious for an affected person. A number of mutations in genes governing these types of perception lead to hereditary defects in humans. But little is known about our sense of touch, where defects might be so subtle that they go unnoticed. In the May 10 issue of PLOS Biology, Gary Lewin’s laboratory at the Max Delbrück Center for Molecular Medicine (MDC) in Berlin demonstrates that differences in touch sensitivity arise from genetic factors that can also be inherited. Some of these factors support hearing as well, meaning that a single mutation may impair both senses.

There are good reasons to suspect that hearing and touch might have a common genetic basis. Sound-sensing cells in the ear detect vibrations and transform them into electrical impulses. Likewise, nerves that lie just below the surface of the skin detect movement and changes in pressure and generate impulses. The similarity suggests that the two systems might have a common evolutionary origin – they may depend on a common set of molecules that transform motion into signals that can be transmitted along nerves to the brain.

In the current study, Lewin’s lab and collaborators at medical schools in Berlin (Charité), Hannover, and Valencia, Spain (Hospital Universitario La Fe) carried out a classical “twins study” to try to discover a hereditary basis for touch sensitivity. The project compared the touch and hearing acuity of identical twins (who have identical sets of genes, including any mutations that might cause defects) with that of fraternal twins, other family members, and a wider set of subjects. They discovered a significant hereditary trend in touch sensitivity, and this correlated strongly to certain types of hearing problems.

“We found a strong correlation between touch and hearing acuity in healthy human populations,” Lewin says. “Additionally, about one in five young adults who suffered from congenital deafness had very poor touch sensitivity.” Blind subjects used as controls, on the other hand, often had enhanced touch perception. This made sense because the genetic basis of vision depends on proteins called photoreceptors that detect light rather than motion.

During the tests, subjects were exposed to vibrations of various frequencies; another experiment had them run their fingers over a fine grating with ridges spaced at intervals of about a millimeter.

One group of subjects suffering from Usher’s syndrome, a hereditary condition that leads to both deafness and blindness, had a significantly impaired sense of touch. This suggests that the gene USH2A, which is mutated in the syndrome, contributes to sensations of both touch and sound. There are likely to be many more genes that play a role in both types of perception.

The scientific literature reports about 60 mutations in known genes that have been linked to hearing impairment, and about 60 more alterations in DNA with a similar effect that haven’t yet clearly been linked to a gene. “Our next task will be to investigate some of these other cases to see if they are also correlated to problems with touch,” Lewin says. “This will give us a better understanding of the genetic mechanisms that underlie both types of perception.”

An earlier study by the labs of Gary Lewin and Carmen Birchmeier at the MDC showed that while defects in touch sensation don’t seem to cause serious problems for people, those affected may be aware of them. “A number of subjects report problems in gripping objects – they may need to watch their hands as they grasp something,” Lewin says.

– Russ Hodge

The full article can be seen for free at:


Preliminary draft of the Minutes from the 9,154,388,279,911,101,314th meeting of the Committee for Intelligent Design

copyright 2012 by Russ Hodge

Preliminary draft of the Minutes from the 9,154,388,279,911,101,314th meeting of the Committee for Intelligent Design

Subgroup: Eukaryotes

Sub-subgroup: Exploratory Committee on Multicellular Organisms

Sub-sub-subgroup:  Worms

Sub-sub-sub-subgroup: Worms with a tubular form


Please make any corrections you see fit before we circulate the final version of the minutes.


Attendance: All 9,453 members of the committee were present; the Head of the Department of Viral Engineering was out with a cold and was replaced by his deputy.

The Big Boss called the meeting to order and introduced the agenda with a plea that presenters stick to their allotted times so that there would be ample time for questions. He noted, with a bit of irony, that he has over seven billion other meetings with other subcommittees to attend, and these all need to take place within the next few minutes. To a proposal that he simply expand the fabric of time to allow for special cases, the Big Boss said, “You can only stretch things so far before things get out of hand; the first four days have already expanded to fill up about 12 billion years. And in my experience, speakers are always willing to talk and talk until they fill whatever time is allotted to them. And I have a vacation planned in three days and I am not willing to postpone the flight another time.” (Discussion closed.)


Minutes of last meeting read and approved.


Continuation of the discussion on Means for Creating Multicellular Organisms.

The Working Group on Worms in a Tubular Form got up to give a PowerPoint presentation with their proposals for a basic body plan. They had, however, saved the presentation in the wrong format and had to run it from an iPad provided by the Biochemistry Department. An appropriate adaptor plug had to be requisitioned from Technical Resources. Then the bulb on the beamer burned out. The Big Boss tapped his fingers impatiently on the table and finally expanded time by ten minutes until things could get straightened out.

During this period the Working Group on bacteria once again raised its motion that unicellular life was fine (supported by the WG on Archaea); they repeated their basic objection to eukaryotes with the claim that once DNA was packed in a cell nucleus, it was especially susceptible to mutations due to the inherent flaws in physical chemistry (noting their previous objection to the creation of DNA) unless you intervened in every chemical reaction and made sure that every single nucleotide was faithfully reproduced. He reported on several cases in which entire regions of DNA had been duplicated, extra chromosomes were acquired, genes were deleted, etc. And that might lead to Evolution, a process which violates the Charter on the Rules of the Universe as Decreed by the Big Boss.

The head of the committee on Eukaryotes pointed out that bacteria likewise underwent mutations, in fact, at a much more rapid pace because the organization of its DNA into circular plasmids permitted them to swap genetic material during S-x.

The representative of the Committee on Occam’s Razor (C.O.R.) once again requested that it should be permitted to pronounce words like S-x without leaving out letters. To which the Committee on Propriety (C.O.P.) replied that in the Charter on the Rules of the Universe as Decreed by the Big Boss, S-x was entered in the Database of Dirty Words.

C.O.R.: Even when it refers to bacteria?

C.O.P.: Yes, they stick those disgusting spaghetti tube things into each other. The only way to stop it is to put them in a blender. You should have listened to us when we objected to S-x in the first place.

The Big Boss gaveled for Order and the Subgroup began its presentation.

Summary: the Working Group proposes a simple, tubular body plan with a mouth on one end and an anus on the other. The form is modular: the head region may be connected to the tail by a number of segments which, for all practical purposes, should be virtually identical. The segments have “nubs” on the side (note to Department of Terminology: create appropriate Latin term) which could be used, at a later date, as the base for filaments or appendages.

Questions raised: Why are the middle segments necessary? Why can’t the thing have just a head and an anus?

Response of the committee: Some system of legs or fibers may be desirable, in new species in the long term, for locomotion, which might be required to find food.

Question: Why can’t the food simply be brought to the worm?

Response of the committee: This is desirable because of previous decisions which made unicellular organisms mobile. As the Big Boss stated during that meeting, “Otherwise everything will have to live on its own dung heap.” And no mechanism had yet been invented to attract food to the creature intended to eat it, except for magnetism, and adding a magnet to the worm body plan and magnetism-sensing proteins to all of its prey would require an unacceptable number of interventions in existing species. And that would be forbidden by the decree under the Charter on the Rules of the Universe as Decreed by the Big Boss: “Once invented, no species may undergo significant changes outside of a standard range of deviation.”

Call for clarification by the Department of Terminology (D.O.T.): We still don’t have a technical definition of the term “species”. (Groans around the table).

The Department chair was reminded that the problem has been referred to Subcommittee.

D.O.T.: Well why is it taking them so bloody long?

(General silence; D.O.T. will be fined at the standard rate for using a Dirty Word; the amount will be determined by the C.O.P. and notification will be sent through the Billing Department. C.O.P. stated: “And this time please provide the correct account number!” The chair of D.O.T. smirked.)

Comment by the representative of the Committee on Flatworms: Why are a mouth and an anus even necessary? Why can’t the worm simply absorb nutrients through its skin, like flatworms do?

Response by the Subgroup: We’ve been over and over and over this; if you want thicker animals you have got to invent a digestive tract and some sort of circulatory system, because due to the nature of cells (casting a dirty look at the chair of the Subgroup on Cells) nutrient molecules won’t simply diffuse to the inner organs.

At this point the Big Boss remembered a note from the last meeting on Flatworms and called for a status update on the Planarium problem. “The d-mned things just won’t die,” he said. “You cut off the head and the tail grows a new one. H-ll, I’ve chopped one up into about 300 pieces and each one of them grows into a whole new worm. What measures are being taken to prevent the things from just covering the whole d-mned planet?”

Response from the rep. of the Committee on Flatworms: We have put in a special application for the creation of several species of predators.

Comment from the Big Boss: “Well, just make sure the predators die. And make sure that when a planarium passes through their digestive system, it gets broken down into molecules. If the cells go through intact we’ll still be stuck with the same problem.”

Comment by the chair of the Subgroup on Dictyostelium: Why can’t the cells of the worm simply disband, seek out food on their own, and then reunite?

Intervention by the Big Boss: “Dictyostelium was an interesting experiment, but it’s hard to find the things when you need one. First of all, they’re so small I can’t see them without my bifocals, and second, you can never tell when they’re likely to group up to form a worm, or one of those dandelion-like things, and those are liable to blow up any time they get hungry.” He requests an update on the Dictyostelium Disaster from the Research and Development department.

Chair of R&D:  We’ve traced the problem to an error made by the Department of Mathematics and Physics; they did not properly calculate the force required by the cell adhesion molecules. Dictyostelium cells only stick together when the system has an optimal level of energy – in other words, when they’ve been fed. The problem was detected too late in the design process without sending the whole thing back to subcommittee or violating the law on standard permissible variation within an existing species.

Comment from the Department of Terminology: (Cut off before the standard request for definition could be made.)

Question from the Subgroup on Technical Innovation: Why is it that every time we invent a new species, we have to stick to the same conservative biochemistry? Why can’t we please, please, just once make an organism from scratch and not have to integrate all these past designs which, if you ask me, makes things way too complicated? Instead of integrating genes from bacteria and archaea into eukaryotes, we should have just junked the past and started over.

Answer from R&D: I quote from the basic Statutes on Biodegradability: “Any new organism which is created must adhere to basic chemical and physical laws and their subcomponents must be degradable by other organisms in the ecosphere as a means of energy conservation.”

Comment from the Chair of Physics: Our calculations demonstrate that violating this principle would require a constant, massive influx of supernatural energy into the Earth environment to support higher life forms on the scale we have planned.

Comment from Astrophysics:  And we would like to state once again, for the record, that when you guys started inventing biochemistry, we told you to make a system that would withstand supernovae. But did you listen? Well, did you??

The Big Boss allowed one final question before moving to adjournment.

The chair of the Subgroup on Multicellular Organisms: We would just like to point out that these meetings take up a vast amount of time. I have consulted with all the Subcommittees and the Head of R&D and the Technical Support Groups and we would like to ask for an amendment, or at least a special waiver, in the Prohibition on Speciation under the Rules of the Universe as Decreed by the Big Boss. Once the basic worm plan has been established, we could just let the rules of chemistry and physics alone and we’d get a plethora of advanced species.

The chair of the Subgroup on Geology points out: For God’s sake, man, the Cambrian period is coming up and you’d get some kind of explosion!

The Big Boss patiently pointed out that Rules were Rules.

The chair asked for a voice vote on the general plan for tubular worms as presented; the majority approved; the chair of the Subgroup on Dictyostelium objected; D.O.T. and C.O.P. abstained. The chair pointed out that C.O.P. didn’t have a vote and couldn’t “abstain”.

The Big Boss said: “Change the record to record that.”

Conclusion: The plan for tubular worms should be submitted to R&D for working out the details. They should present a final proposal at the next meeting, to be held in one minute.

R&D submitted their routine request for an expansion of time because of a heavy workload. “Refer to our minutely report,” the chair said. “Check Appendix 412. We have 8 trillion ongoing projects.”

The request was denied.

The Big Boss stroked his beard, consulted the time in picoseconds on his large, gold pocketwatch, and adjourned the meeting.

“I’m picking up good vibrations”

If you’re reading this on your laptop right now, say over a Venti Latté at Starbucks, take your hand off the hot cup and lay your fingertips for a moment on the keyboard. You may feel the hard drive spinning, or the fan blowing. Your ability to detect heat and vibrations is due to the presence of different types of nerves in your fingertips. A recent finding by the labs of Carmen Birchmeier and Gary Lewin published in the current issue of Science, shows that a molecule that directs the development of nerve cells is important for the detection of vibrations.  This molecule determines the form this nerve cell acquires, its functions in the nervous system, and ultimately whether humans sense high-frequency vibrations. With the findings, the lab has managed to tell a complete story of how the development and function of the nervous system of an organism as a whole can be directly linked to a molecule at work in one of its cell types.

Before scientists can study different kinds of nerves, their functions in organisms, and their roles in disease, they need a way to tell them apart. Hagen Wende and other members of Carmen’s lab first carried out a screen to try to find molecules that could be used to make fine distinctions between types. They discovered that a sub-group of mouse peripheral neurons located in dorsal root ganglia (DRG) produced a protein called c-Maf. Some of the cells expressed this molecule, along with another protein called Ret, at a very early stage. They continued to produce both molecules during the embryonic development of the mouse and after birth.

Some DRG neurons were already known as mechanosensors – transmitters of touch, pressure and vibration sensations – and Hagen and his colleagues wondered about the role of this subset of cells that produced c-Maf. One way to find out would be to “knock out” the c-Maf gene using genetic engineering techniques. Since blocking the production of c-Maf throughout the embryo is lethal – c-Maf has vital functions in other cells – the scientists used a “conditional” knock-out method that removed it only in DRG neurons. The next step was to investigate the effects of this procedure on nerves and the animals’ perception of sensory stimuli.

First they discovered differences in a group of neurons in the DRG: these neurons no longer had thick axons – the trunk-like structures that transmit signals to other nerves. Some of those cells end in thick, egg-shaped ends called Pacinian corpuscles, which detect sensations like pressure and vibration. The corpuscles were much smaller when c-Maf was absent.

“Measurements done by Stefan Lechner in cell cultures showed that the change profoundly disrupted the neurons’ functions,” Carmen says. This effect was very strong in cells called rapidly-adapting mechanosensors (RAMs), which respond to the movement of skin rather than pressure.

Did the changes in mouse neurons correspond to similar effects in humans? “c-Maf also plays a role in the development of the eye – particularly the lens,” Carmen says. “Families with mutations in c-Maf were known to have developmental abnormalities in the eye. But their sensitivity to vibrations had never been tested.”

The researchers contacted one of these families, in whom four people carried the mutation, and tested their ability to detect vibrations. They discovered that the carriers had to be stimulated much more strongly to detect high-frequency vibrations like those produced by the spinning hard drive of a computer, whereas their sensitivity to lower, rumbling vibrations was not affected. And family members without the mutation could detect both types of sensations at normal levels.

Further experiments provided a biochemical explanation of the way changes in c-Maf affected cells. The scientists discovered that the neurons weren’t activating genes called Ret or crystallins (which are crucial in the development of the eye and its lens). They also produced smaller-than-normal amounts of a membrane channel protein called Kcnq4. Gary’s lab has collaborated with the group of Thomas Jentsch at the MDC and FMP to show that this molecule, which permits a flow of potassium ions through the membrane of nerves, plays an important role in the function of mechanoreceptors.

“This provides a full picture of the way c-Maf directs the development of rapidly-adapting mechanosensory nerves by targeting other genes,” Carmen says. “Without it, these cells fail to acquire their proper structure; they lose the Pacinian corpuscles which are needed to ‘fire’ the cells and transmit a signal on to the brain. And humans lose their sensitivity to high-frequency vibrations.”

Link to the full text of the article

Home page of Carmen Birchmeier’s lab

Tipping the balance on Alzheimer’s disease

A mix of math and experiments links a main symptom of Alzheimer’s disease to subtle changes in protein dynamics

In 1906, while peering at brain tissue through a microscope, Aloysius Alzheimer discovered one of the main hallmarks of the disease that now bears his name. The tissue came from a former patient who had just died as a consequence of a severe, progressive form of dementia. Alzheimer found that the space between her brain cells was filled with clumpy “plaques” made of proteins. Their main component is a protein fragment called amyloid-beta peptide, or A-beta. It starts as part of a longer protein called APP that is found in cell membranes. Making the deadly fragment requires enzymes to dock onto APP and make a series of cuts. While this probably happens to some extent in healthy people, it occurs much more often during the disease, and figuring out why is a central question in Alzheimer research. Now a combination of experiments and computer models have provided the labs of Thomas Willnow and Jana Wolf with at least part of the answer. Cutting works best when single APP molecules bind to each other in pairs. In healthy situations, another molecule blocks the pairing and most APP molecules remain bachelors. This discovery, reported in the October 2011 issue of the EMBO Journal, provides a potential new focus for the development of Alzheimer therapies.

 The current study was carried out by postdoctoral fellow Vanessa Schmidt and PhD student Katharina Baum, with Angelyn Lao from Olaf Wolkenhauer’s lab at the University of Rostock. It builds on previous work from Thomas’ group. In 2009 he showed that a protein called SORLA is involved in the development of the disease. This molecule participates in the movement of APP through the cell and the production of amyloid-beta peptide. Its effects are usually beneficial: increasing the amount of SORLA leads to less A-beta, both in the test tube and animal models. Mice that have been genetically engineered to lack SORLA, on the other hand, produce higher levels of the dangerous amyloids. But the reasons have been unclear.

The processing of APP involves an interplay of so many proteins that a “systems biology” approach, using mathematical modeling, was necessary to describe their roles. “Most mouse models and other studies have used ‘all-or-nothing’ methods, either completely eliminating particular molecules, or raising their amounts to unnaturally high levels,” Thomas says. “Patients experience much subtler changes in protein levels. We needed a way to make small changes in protein expression and watch their effects over long periods of time.” Levels of SORLA drop in many Alzheimer’s patients, but it isn’t completely lacking.

The scientists developed a unique cell-based system in which they could incrementally raise or lower concentrations of APP and SORLA. Then they carried out quantitative studies to study the effects of the changes on the production of amyloid-beta peptides. The next step was for Katherina, Jana and their colleagues to replicate these effects in mathematical models.

A breakthrough came when the scientists applied “Hill kinetics” to the problem. This approach detects cases when the elements of a system produce an effect by cooperating, rather than acting independently. It showed that the production of A-beta depended on some sort of cooperative event, which further experiments exposed as the pair-wise binding of APP proteins.

“This pairing creates an optimal ‘platform’ for enzymes to bind to APP, the first step in producing dangerous fragments,” Thomas says. “That discovery gave us a hint about the role of SORLA. It doesn’t directly stop enzymes from binding to APP, which was one of our early hypotheses. Instead, it interferes with the pairing of APP molecules. It locks up single copies so they don’t bind to each other. This means fewer ideal ‘docking sites’ for the enzymes, and a lower production of A-beta.”

The cell culture method allowed the scientists to observe the effects of a gradual raising or lowering of levels of SORLA. Even small reductions led to significant jumps in the amount of A-beta. “This helps explain how a drop in SORLA of just 25 percent in some Alzheimer’s patients leads to dramatically more fragments,” Thomas says. “It’s due to an increase in the cleavage of APP. Other groups have shown that APP normally forms pairs about 30 to 50 percent of the time. If levels of SORLA drop, that proportion rises. Cells produce more amyloid-beta peptide, leading to accumulations and the dangerous plaques seen in Alzheimer’s disease.”

The study has implications for the development of new therapies, he says. Rather than trying to inhibit the activity of APP-cutting enzymes, which healthy cells might need for other reasons, scientists can look for drugs or other substances that imitate the action of SORLA and block the pairing of APP molecules.

“This is the first mathematical explanation of the anti-Alzheimer effects of SORLA,” Thomas says, “and it helps show how relatively small changes in the ‘dosage’ of this molecule can have big effects on the course of the disease.”


Schmidt V, Baum K, Lao A, Rateitschak K, Schmitz Y, Teichmann A, Wiesner B, Petersen CM, Nykjaer A, Wolf J, Wolkenhauer O, Willnow TE. Quantitative modelling of amyloidogenic processing and its influence by SORLA in Alzheimer’s disease. EMBO J. 2011 Oct 11;31(1):187-200

Link to the original article