Casalinghe Porche Pic

playground Bioinformatics

With all the many useful tools that produce the bioinformaticians to us to facilitate the work of biologists, we have now reached a point also allows the interested layman a playful introduction to the mountains of data.

A very good example is the Genome Projector , the genome data from many (so far) bacteria using the familiar Google Maps interface represents.
The reference genome of the laboratory strain K12 of Escherichia coli (easy to find in the list, it is already marked with a bar) is a good starting point for anyone who wants a look take a look. Who in the pathway map to find the citric acid cycle?

Transfer Pokemon From Diamond To Soul Silver

And yet I'll say! What

Unexpected Evolution
Sonja of Brethorst, Press and Public Relations
University of Veterinary Medicine Hannover
26/01/2009

Higher animals do not come from the lower animals from
scientists at the University of Veterinary Medicine Hannover (Veterinary Medicine), the Sackler Institute for Comparative Genomics at the American Museum of Natural History and Yale University will present the latest edition of the online journal PLoS Biology surprising results of evolutionary research. The publication is available from Tuesday, 27 January 2009, http://biology.plosjournals.org be viewed on the web.

The German-American working group challenged with their research, the current view of the progress of evolution of animals. So far it was taken for granted that the evolution of animals from simple to complex animal strain was. The new research shows, however, that the lower animals have developed in parallel with the higher animals. Among the lower animals such as corals and jellyfish are counted, the higher animals include all known groups of the worm to man.

press release from the Information Service Science

Did not I just say? In a few sentences, both the old story with the scala naturae , and an interesting classification of animals into two groups - higher and lower. Here at least the border at a known location is taken, with the higher animals are the Bilateria meant. But why then do not say Bilateria?

In the comments to my last post on here I have quoted from papers that draw the line between higher and lower animals somewhere else, such as in vertebrates. The whole thing makes sense in any event no.

And now I shall finish with stealing from T. Ryan Gregory of Genomicron , who has the paper also excitedly

"It is absurd to talk of one animal being higher than another" (Charles Darwin, 1837)

Coopers Home Brew Yeast

elite universities can now spend all the money

I go on average once per day from the office / laboratory (the tower in the background) back to our experimental greenhouse (a few hundred yards behind me) and. Until now you could save valuable seconds on this track by abridging the trees. What many people do at the university, the trail is not just me! Now the university has probably something about it that her well-kept lawn English their natural state Unkrautbeet is entered, and has set up a barrier. But much more hats to be related not just to the right of the image that is already created a new starting ;-)

Gallery Female Genetalia

project Paper Summary # 2: The RTR complex in plants?

And here, the discussion of our latest papers! While in part 1 keep a little background for the genes / proteins, went off tonight into the plant genome and the question is whether these RTR complex in the model plant Arabidopsis thaliana .


make the most of our work with insertion mutants. These are plants in which using the soil bacterium Agrobacterium tumefaciens relatively large DNA fragments were introduced into the sequence of a gene. This leads ultimately to the fact that the protein product of this gene can not be established, the plant line is distinguished from wild-type plants only in the fact that a particular gene was turned off. The purpose behind the investigation of these knockouts is quickly evident: When comparing wild type and Knockoutlinie, it is very likely that any additional defect is in the Knockoutlinie on the failure of the gene. Now you have to rethink just yet - the failure of a gene leads to certain failure, then this gene is normally fulfilled this specific function that prevents the development of the defect.

First, it is natural to ask: Is it the genes of the RTR complex at all in Arabidopsis? Here, you can now save a lot of work, thanks to very good bioinformatics and the freely accessible genome databases of many organisms. What we found is a good fit to the previously described genes, particularly from the yeast Saccharomyces cerevisiae and man.
RMI1 for the gene (or BLAP75) there are two possible candidates Arabidopsisgenom. One of them (the gene At5g19950 ) seems to be not expressed, and examined by us insertion mutants were completely normal. It could therefore be a pseudogene . The second candidate ( At5g63540) was all the more interesting, as I will show today and in the following posts to our papers. This gene was therefore named AtRMI1 of us [1].
on the T from RTR - the topoisomerase. Here it was easier because of TOP3 or a homologue TOPO3α was only one candidate gene in question, or At5g63920 AtTOP3α.
A little more complicated it is for the RecQ helicase. In this family we already know that there are seven members in Arabidopsis. Which of these seven now but the functional homologue to the only RecQ helicase in yeast, SGS1? In humans, this is among five family members of the BLM gene, and armed with the development of these two genes already covered some of the RecQ helicases Arabdopsis out. Of the rest, then remains only RECQ4A ( At1g10930) left when we include already known properties of members of the RecQ family in Arabidopsis with a (Hartung et al., 2007).

Fortunately for these genes were then also available insertion mutants, we were able to work with.

Finally now some "real" data. The description of how and why certain genes have been found at all and used, and how the mutants are built is certainly an important part of a paper - it's a bit boring.
There is a relatively simple method, the involvement of a gene or its protein product from the DNA repair study: Intentionally damaging the DNA, then these damages are repaired. But a gene is turned off, which is involved in the repair of DNA, then the repair does not logically so well. This can be measured in different ways, we determine the relative fresh weight of seedlings treated compared with untreated same old seedlings. For problems of DNA repair result such as death of the affected cells, which can then no longer part or waxes. The result: Smaller, lighter seedlings.
The range of possible damage to DNA is incredibly high, accordingly, it is also a lot of repair pathways. By the organisms various substances with known harmful effects on the DNA is exposed if you can make with this experiment is also a first classification of the studied genes in these repair pathways. A Knockoutmutante Namely only more sensitive than the wild type response to a substance if it is active in the repair pathway is affected.

Figure 3 from Hartung et al (2008)

In this figure, the sensitivities of Knockoutmutanten Gene RECQ4A, TOP3α RMI1 and shown to various mutagens. Against methyl methanesulfonate (MMS, A in the figure), many genes in homologous recombination are sensitive, so our three genes. MMS generates Adducts in DNA by a methyl group attached to nitrogen atoms in the bases of DNA. This has to mean that the normal double helix is distorted, and basic processes such as transcription and replication can not take place. This is probably also related to the homologous recombination, as it assists directly to resolve problems at the replication fork. Apart from this damage by alkylation but also by the repair pathways of base excision repair and nucleotide excision be resolved [2]. The inaccuracy of these paths leads the way through the detour of mutations in a cancer-promoting effects of MMS.
cisplatin (cis -specific Diamindichlorplatin, B in the figure) is an interesting material. About the rather accidental discovery of this small molecule I have already written . Today it is one part of one of the most commonly used chemotherapeutic agents, on the other hand, however, the most studied substances in terms of the mechanisms of DNA damage. What happens when cisplatin enters the cell? The central platinum atom reacts happily with just about any molecule that gets it hands on. Therefore, one then finds Platinaddukte of sugars, fats, proteins, but also the DNA. Stupid thing is though, that cisplatin on his two chloride groups can also react twice, and thus two previously unconnected Molecules covalently linked. So then ever proteins bound to DNA, or even worse, two bases of DNA covalently linked. This is called cross-linking, and there are two possibilities: either two bases from different strands of DNA are linked (= interstrand cross-link), or two bases are linked within a line (= intra-strand cross-link). The latter is more frequent in the cisplatin product, and here the nucleotide excision repair tasks are in and the homologous recombination (particularly during replication). Last
still camptothecin (CPT, C in the figure). This is an alkaloid from the plant such as Camptotheca acuminata is made for pest resistance. And the pests that nibble on the plant do'm really sorry: In the previous part I have just described what makes a topoisomerase to the DNA. Hinder this process of camptothecin topoisomerase first Just in the state when TOP1 is covalently linked to the DNA and there is a single strand break in DNA, CPT binds to it and prevents the topoisomerase closes the gap and come off the DNA. As a result, the replication of a hand, a protein linked covalently to the DNA is located and disabled the replication proteins, and also that by the sudden unwinding of the double strand of this gap in the DNA a double-strand break is. Major problem and most likely the death of the hungry pests [3].

As you can see, all mutants more sensitive than the wild type (Col-0 in the figure) to MMS and cisplatin. Against CPT contrast, only the Knockoutmutante of TOP3α is sensitive, the other two do not. top3A-2 reacts strictly speaking also on MMS and cisplatin sensitive than recq4A-4 and rmi1-2 . While these sensitivities, one of the most common indications now that the three proteins perform their functions together (that may be in a RTR complex) to interpret the results also indicate a special role for TOP3α. will on the I received but in the next or the next post - with NEM Cliffhanger have to return it that easy?


[1] So really new and creative name gives the genes rather rare, but it does happen. See, for example, the gene and its antagonist SUPERMAN KRYPTONITE ...
[2] If I start now to describe in detail each repair pathway I will not even finished the post. I have here, however a nice idea: I could devote the mutagens own posts, and then enter it on the relevant repair pathways.
[3] The camptothecin-producing plants have way TOP1 genes with slightly different sequences, so that even nicht anfällig gegenüber CPT sind (Sirikantaramas et al, 2008).

Masterbation Tecneaks

Edgar Allan Poe

Heute vor 200 Jahren wurde der amerikanische Schriftsteller Edgar Allan Poe geboren.

It was many and many a year ago,
In a kingdom by the sea,
That a maiden there lived whom you may know
By the name of Annabel Lee;
And this maiden she lived with no other thought
Than to love and be loved by me.

I was a child and she was a child,
In this kingdom by the sea:
But we loved with a love that was more than love —
I and my Annabel Lee;
With a love that the winged seraphs of heaven
Coveted her and me.

And this was the reason that, long ago,
In this kingdom by the sea,
A wind blew out of a cloud, chilling
My beautiful Annabel Lee;
So that her highborn kinsmen came
And bore her away from me,
To shut her up in a sepulchre
In this kingdom by the sea.

The angels, not half so happy in heaven,
Went envying her and me —
Yes! — that was the reason (as all men know,
In this kingdom by the sea)
That the wind came out of the cloud by night,
Chilling and killing my Annabel Lee.

But our love it was stronger by far than the love
Of those who were older than we —
Of many far wiser than we —
And neither the angels in heaven above,
Nor the demons down under the sea,
Can ever dissever my soul from the soul
Of the beautiful Annabel Lee:

For the moon never beams, without bringing me dreams
Of the beautiful Annabel Lee;
And the stars never rise, but I feel the bright eyes
Of the beautiful Annabel Lee;
And so, all the night-tide, I lie down by the side
Of my darling — my darling — my life and my bride,
In her sepulchre there by the sea,
In her tomb by the sounding sea.

Annabel Lee, von Edgar Allan Poe

Dies ist das letzte von Poe verfasste Gedicht vor seinem frühen und mysteriösen Tod 1849. Es ist einer der (Probably including The Raven, but the poem to know many yes) Texts of Poe, which touch me most. Most likely it is addressed to his wife Virginia - it was the latest in a series of Poe related women, which he lost by TB. One of Poe's short stories, the mask of the Red Death (The Masque of the Red Death), referring probably to tuberculosis and the time of publication it suffering from Virginia. I find it fascinating that two of the main themes of Poe's texts - Women and death - even his life in a way impressed that it had one of his short stories have been.

stumble In keeping with tradition, I use a good cognac and three red roses leave.

Poe in German (Project Gutenberg-DE)
Poe in English (Project Gutenberg)
Poe to listen (Librivox.org)

5 Weeks Cervix Hard And Low

Why you should have at least intermediate level knowledge of science, if you are out medical press releases ...

... or: Gene, Gene, Gene and the evil junk DNA!

This is again a good example of why I usually refrain to read press releases. A research group has shown in a recent paper in Nature that can help microRNA (miR-21) for disease of heart muscle disease. The interesting thing is that they connect showed between one of the many gene silencing mechanisms and a human disease. Mind you, this compound has long been known, as the authors themselves write already in the abstract of the article. So far everything is still OK.

But what makes the press office of participating in the work of Rudolf Virchow Center of it?

"genetic garbage" triggers heart muscle weakness from

Würzburg, 30.11.2008. Tiny fragments of the genome - so-called "micro-RNAs, which until recently were regarded as unimportant, could now revolutionize the prevention, diagnosis and treatment of heart failure. Würzburg researchers found such a first time in the heart, they blocked and thus could not only protect endangered mice before the onset of the disease, but also to heal diseased heart muscle disease mice. The results describe the scientists of the University of Würzburg in the prestigious science journal Nature.

The decoding of the human genome took a surprising message with it: Only about 1.5 percent of the total genetic information is needed for the production of our proteins, where the genes are a kind of copy that messenger RNA transcribed into proteins. The rest of the genes was long regarded as meaningless "genetic garbage" because their RNA without significant Function was. In 2006, however, for the discovery that RNAs, from which no proteins, important functions in the body of the Nobel Prize for Medicine awarded have [sic]. These RNA fragments regulate the formation of the proteins directly binding to the messenger RNA. Is something wrong, the body produces for example, too much or too little protein, the unit cell of the body out of balance - caused diseases.

The press release goes on, but deals with this seemingly very interesting topic but no more. Maybe because it was known in the press office nothing more pro-depth than this superficial blah?
Let's go the whole thing from the front to the rear. The title is already great, "genetic garbage" in the same scare quotes , and somehow it sounds as if at last the ultimate cause of heart failure was found. On the genetic garbage, so the junk DNA, I would be talking in more detail, now only time will unravel the message.
First movement - microRNAs (again scare quotes) are by no means "fragments of the genome," and they were not until recently as unimportant. Rather, microRNAs as well as all other genes (including those that code for proteins) is first transcribed times, ie, a copy of the gene in the form of RNA produced. When genes are called proteinogenic this RNA, mRNA (messenger RNA). When genes for microRNAs, well, microRNA halt. Would it really fragments of DNA, it would be one part microDNA, and the other, the cell would be dead (broken chromosomes and so). A quick search on PubMed also show that at least written since 2001 about microRNAs - not "recently" so. Let us not only this subfamily of regulatory RNAs, but the whole process of gene silencing , then the statement is even more ridiculous. About post-transcriptional gene-silencing is then written since 1955 (with almost 19 000 articles published to date), and on the information side e for the (in the press release so explicitly mentioned) Nobel Prize (Fire and Mello, 2006) is taken directly relating to work in plants and fungi in 1990.
In the second paragraph then goes merrily Keep it up. Since the text is contrary to first violent. On the one hand, to be only 1.5% of the genome genes ("for the production of our proteins required"), on the other hand, the rest of the genome is probably full of genes ("The rest of the genes")!

This sentence is full of errors anyway:

The rest of the genes was meaningless as long as "genetic garbage" because the RNA was no significant function.

So, no definition of what a gene. Actually, even an admission since the 7th who paid attention in class not to biology class. Taken literally, the author apparently assumes that the 98.5% of the genome (because they supposedly genes) are transcribed in RNA. This happens, for the most part, but not - the genome is transcriptionally mostly dead Even more important, so far no one has claimed that once produced RNA did not function [1].

now to the junk DNA. Whenever in recent years, someone has an effect that is not the schema gene - mRNA - protein follows, he has the same evil unpacked junk DNA. Accordingly, so are all other molecular biologists so limited that everything in the genome, which is not that simple Scheme corresponds to dismiss as genetic garbage lying around the completely unnecessary and complicates the search for genes. But now comes the underdog, who confronts his great new discovery to the narrow-minded scientific establishment. Sure, that is so taken up a representation by the media like.
With this view, there is only one problem: it is wrong, and almost as long as we even know that there are genes and the DNA is the genetic material in the cell. Only a few years after the description of DNA structure by Watson and Crick in 1953, was the translation informed, in essence, that the production of proteins from the information of the mRNA. This was already clear that for RNAs this process are needed, none of which proteins are produced: the tRNAs and rRNAs. Also, the fact everyone learns in school. The basic assumption, non-coding RNAs with a function in the cell would be known only for a few years ago, is not only wrong - these RNAs are part of the establishment!

That is one aspect. The other side has the definition of the concept of junk DNA to do. First of all is not "waste" of which we do not know the function. With junk DNA elements in the genome are known, which have proven does not function! The Nobel laureate Sydney Brenner are in this video on iBioSeminars (from about 11:20) a very good Example. The Alu sequence is with a length of about 300 base pairs in the human genome into millions of copies before they do with it, depending on the estimate of 10-30% of the entire human genome! Function? No way! In the end, Alu elements parasites of genetic parasites.
So-called transposons are genetic elements that are specific sequences at their ends and encode between genes whose protein products recognize these endings and set there cuts in the DNA. A transposon can thus cut and paste your site in the genome of a hike to another. A benefit to the host genome, the first no, transposons use it only as a delivery vehicle. Alu elements and other similar sequences go this one step further: In order to carry genes themselves are too small. On their end but they also have the sequences that are recognized by the Transposonproteinen. Alu elements are therefore ex-transposons, which have saved the effort with the genes and use their still functioning Transposonkollegen. Again, however, no direct benefit to the host cell.
Larry Moran has in recent months, various elements in the human genome listed who have secured not function, that fall within junk DNA. The Alu elements are (listed under SINEs) also there. Overall, he is now, without details of all types of non-functioning elements in the genome to have more than 50% of the size of the genome - and that is a very conservative estimate!
points in the above video Sydney Brenner also points to a widespread misunderstanding of what the term concerned junk DNA. With junk is not meant in English namely the garbage that you throw it away. a better translation would be the word junk , according to Brenner things you can do just not that why do you store in the attic.

Most of the genome appears to be Unnecessary, it is - if you like - call it rubbish. Now as you well know, there are two kinds of rubbish: The rubbish you keep, Which we call junk, and the rubbish we throw away, Which we call garbage.

This understanding of junk DNA triggers on a frequent criticism directed against it in pleasure, just because we see no benefit for these elements is present, that does not mean that these sequences may be used at some point it!


[1] of the current debate on stochastic transcription and benefits of the resultant RNA apart.

Hdloader Hd Not Found

Paper Project Overview # 1: The RTR complex helps turn

Unfortunately there were not many responses to my question if I should report on a recent paper in which I am co-author, here. The poll in the sidebar is clicked exactly 1 time. Since the result but now at 100% for the explanation is, I will continue to do so. Only I will, as Caesar wrote in the comment section, to forgo a research setting at blogging. Their policy does not writing their own papers, but still seems not to be acceptable.
As used in the paper several points to language that can stand on their own legs, I will divide the discussion of the paper. So that is not a mega post, and I can each respond better to the background.

Today I begin the short paper for the relevant genes and their protein products to imagine that everyone has an idea about their function in the cell. Central here is a complex of three proteins, have on their own entirely different biochemical properties.

About the family of RecQ helicases I've written very little, although I am concerned since my graduate work with them. From the Biounterricht some may remember the term for a helicase protein that is required for the copying of DNA (replication). Since the two strands of DNA are stored together, it can be copied only when the base pairings were released. This is achieved by a group of proteins called helicases, which make in energy consumption of a double strand two single strands. After that then start the merry-copy DNA. Helicases but are used not only during replication - most events at the DNA need the help of a helicase, which is why it is of the human genome also according to the UniProt protein database over 150 . Attention has been paid a little more intense with the metabolism of DNA, then it is almost inevitably a family of helicases (ie a group of proteins whose genes are evolutionarily related and all of a single gene have a common ancestor), the RecQ helicases. This is because members of this family of various tasks in the preservation of DNA, as we know it have the following: They are active in recombination and repair of DNA, can be found at the ends the chromosomes, the telomeres, where they contribute to the preservation of these structures and thus prevent such as a rapid aging of our cells. Other family members are true functions in gene silencing (also known as the phenomenon of RNAi was awarded the 2006 Nobel Prize). RecQ helicases biochemically fulfill these functions in general, by recognizing specific DNA structures [1], and they dissolve in energy consumption again. If these functions in animal cells that then can develop cancer.
The vast majority of single-celled organisms have exactly one RecQ helicase, which fulfilled all-rounder, most of these tasks. Interestingly, but also complicate it in multicellular organisms, because they carry several genes for RecQ helicases in their genomes, which have divided the tasks among themselves. People such as 5, even 7 Arabidopsis RecQ genes. A fairly well-studied family member in humans is called BLM, because the mutation can trigger devastating hereditary disease Bloom syndrome . Functionally equivalent to the gene in Arabidopsis RECQ4A. Both suppress the recombination and are involved in certain types of DNA repair. At least one of these tasks are performed in the RTR complex, at issue today. Therefore I will let it also be good for now.

The second protein in the complex is a topoisomerase. It is TOP3 in the yeast, in multicellular TOPO3α called eukaryotes. Topoisomerases solve topological problems of DNA - that's why the name. A simple example will help to understand what was meant by this: Imagine a rubber band before, puts an end to its fixed to a door handle, the other you hold in your hand. Now twist (turns on) its the rubber band. How can resolve this over-rotation again, if the ends are firmly established? The DNA that is slightly easier than with a rubber band, but that is exactly what topoisomerases: cut a line through at this position, the rubber band / DNA now rotate freely. If the over-rotation was dissolved (this is done by the stored energy in the overturning of itself) includes the topoisomerase again the gap. A cut and glued rubber band would probably not use more, but this means only in the DNA, releasing and linking a bond in the molecule, which then makes no difference [2].

The third partner is complex in the yeast and human RMI1 BLAP75. Unlike the first two proteins, it seems to have no enzymatic function. Nevertheless, the complex is doing its job well if you remove this protein from it. This is probably because RMI1/BLAP75 time promotes the recognition of and binding to specific DNA structures, and other helicase and topoisomerase in the complex together. On This allows the two proteins fulfill their tasks cooperatively.
was shown recently that the complex also contains a protein called RMI2/BLAP18. This is closely related to RMI1, and both are complementary in their function. Moreover, it is already known that other, previously unidentified proteins are contained in the complex.

Because of the three core proteins of the complex but received its name - BTB for BLM, and TOPO3α BLAP75 in man or RTR for RecQ helicase, in the yeast TOP3 and RMI1. Exactly what he does with the DNA, I will go out in a separate post. Shortly I will mention only that the RTR complex recently, the sad Honor has been misused by creationists as "argument" to be .


[1] Anyone who has ever wondered where the nearest post of the series remains in DNA structures - guilty as charged. It's not like that because I ran out of topics. It goes further to soon, I promise!
[2] There is a second form of topoisomerases. The cut not one but two strands of DNA by. This is about necessary if more chromosomes are knotted together.

Vegeta Motorcycle Helmet

brain, and in the laboratory

there for many routine tasks in molecular biology laboratory today by many manufacturers kits. You have to isolate DNA? No problem, open your box, take a Some small plastic thing, then so much solution X on it by centrifugation, Y solution on it, done. That has to make over the old method of all yourself, of course advantages:
The results are generally reproducible, we have to handle no more dangerous chemicals such as phenol or chloroform, it is also faster.
The problem: Just because you no longer even works with chemicals, but only used ready-made solutions with meaningless names, many people do not know the application behind the kit chemistry. It will stop just proceed to rule. A second side effect of the kit is the lower yield. A good example to me is Next Generation Sequencing untergekommen:

In the new issue of Biotechniques, a paper by Maricic and Pääbo (login may be required) describes how a change to the standard 454 sequencing protocol can dramatically increase the size of the library of DNA that goes into the actual sequencing reaction.

The trick used is to replace the last step in the library preparation where single stranded DNA is released from streptavidin beads. The original 454 protocol employes NaOH denaturation for this step, but the researchers found that this procedure results in a loss of over 99% of the DNA . However, When they replaced the NaOH denaturation with a heat denaturation by incubation recovery increased to 98%.

These authors are coming from the ancient DNA community and have an obvious motivation for optimizing the DNA retrieval from ancient biological material scarce. However, these findings are equally important to other applications Aimed at sequencing small volumes of biological material tested as tumors and within-host sub-populations of pathogens.

(Emphasis added.)

Wow. I'm used to that after DNA purification, only 50% rauszubekommen back, but> 99% loss? I'm speechless. 454 is one of Roche, and since none of the works will be paid to optimizing a process before it is released to customers? I wonder just how many people probably spent money on failed 454-sequencing have, and the reason was only one problem with the preparation of the DNA rather than the scientific question.


Maricic T, and Pääbo S (2009): Optimization of 454 sequencing library preparation from small amounts of DNA sequence permits determination of both DNA strands. BioTechniques 46 (1) :51-57.


(Actually I did last night, so post the paper review, then I have but a great recipe for peanut butter-chocolate brownies found which would test out I prefer.'s Why you get only used this short post.)

Herpes Inside Nose Treatment

This warm feeling in my stomach

No, I did not just NEN Döner squashed. My concern is one of the reasons why at least I'm in the science (and I assume that this reason is also true for many others).
who speak at the forefront of science research, which has from time to time an edge over the rest of humanity: from the experiments gives interesting data that tell a little about nature. Whenever that happens, the only one in the world is the white, and it's a great feeling, be it ever so small and insignificant. This makes sense in any event all the months of x-times repeated routine laboratory work up for that, one is filled with an indescribable zest, so that one spends more time in the lab as usual was not just me so - wie es aussieht hatte Alex Palazzo vom Daily Transcript dieses Erlebnis gerade , nur ne Nummer größer!

So I isolated each factor and sent them to be identified by mass spectroscopy. Then I waited. Christmas came and went. Friend visited from New York, family visited from Montreal and then early on New Years Eve I received an email from the mass spec facility. My results had arrived! Before anyone was up, I looked over the list and realized what I had stumbled into. I couldn't believe my eyes. It's obviously the answer. Obvious. I should have gone fishing earlier. Now all that is missing is the last piece of the puzzle. That last factor that must link all the bits together.

This is why I haven't been blogging. This is why it's 10:01 PM and I'm in the lab This is why I've been totally obsessed with my work.

This is why I'm in science.

Mrs Brazilian Grandma

good for the ears

If I link to good blog posts, then why not on good podcasts that come between my ears? This should therefore develop in a kind of series ...
This week, I may as well start with three tips:

is the always excellent Futures in Biotech podcast interviews in the current Episode 37 [ MP3 Link ] Marty Chalfie, one of three this year's Nobel Prize for Chemistry. This episode is about his work on the model organism Caenorhabditis elegans and the study of the molecular basis of touch. In the next episode then, the development of GFP as a tool to be addressed, for which he was awarded the Nobel Prize.

StarShipSofa is the audio version of Science Fiction magazines like Asimov's or Astounding. Besides various sections of fiction, such as poems and short stories, there are also non-fiction sections. As a result, Aural Delights 57 [ MP3 Link ] JJ Campanella is a very good overview of genetically engineered crops - informative but exciting, with no hype and panic, but very balanced. At about 55:30 on the part begins.

BBC Radio 4 In Our Time is with my opinion the best history podcast. This is perhaps because that is not picked in the history book as a date or event, and is then listed what happened. Rather, each episode is taken in one aspect or idea of philosophy, science or other areas, and considered in the development over time. Currently, there is the occasion of Darwin in 2009 only in Podcast Feed a four-part documentary on the life of Charles Darwin - great! Online are already three parts [Part 1 MP3 Links , Part 2, Part 3 ].

If you have heard something good, step right up and the recommendations!