Transcriptional Control of Mitosis: Deregulation and Cancer
Research over the past few decades has well established the molecular functioning of mitosis. Deregulation of these functions has also been…'
DEREGULATION of this process is necessary because this NATURAL process would not allow a man-made vector to insert------what is important in this discussion of RANDOM insertion vs SAME-SITE INSERTION is this: the DNA strand has hundreds of GENE SETS ---CODONS -----some are heavily involved in passing genetic traits-----much of these strand codons are INACTIVE or SUPPORT CODONS------this is what NONSENSE REGIONS of our DNA strands are called.
When we read an article saying a research process was successful--------RANDOM insertion of a man-made vector occurred-------that it occurred because of DEREGULATION of a region of a DNA strand-----it is VERY LIKELY that manufactured insertion occurred in what is called JUNK DNA.
Deregulating an area of DNA tied to JUNK DNA is completely different than deregulating regions of VITAL DNA GENES because those regions are SUPER-SENSITIVE to changes whether in physical changes to DNA strand ----or cell environmental/chemical changes in cell.
'The Blueprint of Life
Every cell in your body has the same "blueprint" or the same DNA. Like the blueprints of a house tell the builders how to construct a house, the DNA "blueprint" tells the cell how to build the organism. Yet, how can a heart be so different from a brain if all the cells contain the same instructions? Although much work remains in genetics, it has become apparent that a cell has the ability to turn off most genes and only work with the genes necessary to do a job. We also know that a lot of DNA apparently is nonsense and codes for nothing. These regions of DNA that do not code for proteins are called "introns", or sometimes "junk DNA". The sections of DNA that do actually code from proteins are called "exons"'.
What is important in a very basic discussion of DNA BASIC SCIENCE to to know this: RANDOM INSERTION had as a research goal of simply getting a man-made gene vector to IMPLANT onto a DNA strand then to see if DNA TRANSLATION/TRANSCRIPTION would naturally carry that inserted gene code.
WE HAVE NO PROBLEM THINKING THAT THIS GOAL WAS REACHED.
17 July 2017
At least 75 per cent of our DNA really is useless junk after all
By Michael Le Page
You’re far from a perfect product. The code that makes us is at least 75 per cent rubbish, according to a study that suggests most of our DNA really is junk after all.
After 20 years of biologists arguing that most of the human genome must have some kind of function, the study calculated that in fact the vast majority of our DNA has to be useless. It came to this conclusion by calculating that, because of the way evolution works, we’d each have to have a million children, and almost all of them would need to die, if most of our DNA had a purpose.
But we each have just a few children on average, and our genetic health is mostly fine. The study therefore concludes that most of our DNA really must be junk – a suggestion that contradicts controversial claims to the contrary from a group of prominent genomics researchers in 2012.
Junk or not?
When researchers first worked out how DNA encodes the instructions for making proteins in the 1950s, they assumed that almost all DNA codes for proteins. However, by the 1970s, it was becoming clear that only a tiny proportion of a genome encodes functional proteins – about 1 per cent in the case of us humans.
Biologists realised that some of the non-coding DNA might still have an important role, such as regulating the activity of the protein-coding genes. But around 90 per cent of our genome is still junk DNA, they suggested – a term that first appeared in print in a 1972 article in New Scientist.
But throughout the 2000s, a number of studies purported to show that junk DNA was nothing of the sort, based on demonstrating that some tiny bits of non-coding DNA had some use or other. These claims proved popular with creationists, who were struggling to explain why an intelligently designed genome would consist mostly of rubbish.
The grandest claim came in 2012, when a consortium of genomics researchers called ENCODE declared that, according to their project, a huge 80 per cent of the DNA in the human genome has a function. “They had spent $400 million, they wanted something big to say,” says Dan Graur of the University of Houston.
Graur is one of many researchers who didn’t believe ENCODE’s claim. The heart of the issue is how you define functional. ENCODE defined DNA as such if it showed any “biochemical activity”, for instance, if it was copied into RNA. But Graur doesn’t think a bit of activity like this is enough to prove DNA has a meaningful use. Instead, he argues that a sequence can only be described as functional if it has evolved to do something useful, and if a mutation disrupting it would have a harmful effect.
Millions of children
Mutations to DNA happen at random for several reasons, such as UV radiation or mistakes made when DNA replicates during cell division. These mutations change one base of DNA into another – an A to a T, for example – and when they occur in a gene are more likely to be harmful than beneficial.
But we each have just a few children on average, and our genetic health is mostly fine. The study therefore concludes that most of our DNA really must be junk – a suggestion that contradicts controversial claims to the contrary from a group of prominent genomics researchers in 2012.
When we reproduce, our children inherit a shuffled bag of mutations, and those with a collection of particularly bad ones are more likely to die before having children of their own. This is how evolution stops bad mutations building up to dangerously high levels in a species.
Following Graur’s logic, if most of our DNA is functional, we would accumulate a large proportion of harmful mutations in important sequences. But if most of our DNA is junk, the majority of mutations would have no effect.
Graur’s team have now calculated how many children a couple would need to conceive so evolution could weed out enough bad mutations from our genomes as fast as they arise. If the entire genome was functional, couples would need to have around 100 million children, and almost all would have to die. Even if just a quarter of the genome is functional, each couple would still have to have nearly four children on average, with only two surviving to adulthood, to prevent harmful mutations building up to dangerous levels.
Taking into account estimates of the mutation rate and average prehistorical reproduction rate, Graur’s team calculated that only around 8 to 14 per cent of our DNA is likely to have a function.
Less than an onion
This ties in nicely with a 2014 study that compared our genome with other species and concluded that around 8 per cent of it is functional.
“The findings are entirely supportive of one another,” says one of the authors of the 2014 study, Chris Ponting of the University of Edinburgh, UK. “We are walking around with a genome where only 1 in 10 bases actually matters.”
We don’t know how much of our DNA has a non-sequence-related function, says Ryan Gregory of the University of Guelph in Canada. Some regions of DNA are useful without having an important sequence, so mutations in these areas probably don’t matter. But even taking this into account, most DNA is probably junk, says Gregory.
The challenge for those who think most non-coding DNA is vital is to explain why an onion needs five times as much of it as we do, says Gregory. “I would like to think that most knowledgeable biologists who properly appreciate evolutionary theory and genomic diversity are well aware of the many problems with ENCODE’s claim,” he says.
But most people and even some scientists are uncomfortable with the idea that most of their DNA is junk, says Ponting. Even worse for such people, other genomic studies are now revealing that we all carry plenty of mutations that affect both our coding DNA and non-coding DNA. While evolution weeds out some of the worst ones, this doesn’t stop plenty of mutations collecting in our genome.
“We are walking around as individuals with relatively large numbers of our genes not working properly,” he says. “These are ideas some find shocking.”
'A new transgenic mouse model generated by random insertion of foreign DNA may provide a boost to your current research'.
This is the second problem with these "scientific" research: the scientific method and centuries of validated scientific basic science REQUIRES that VARIABLES in these studies be neutralized or removed in order to PROVE that the scientific study of vectors actually CREATED the results from the study.
What we read over and over and over again in these corporate R AND D studies is ------those newly inserted MAN-MADE gene vectors, for example CANCER VECTORS, actually REDUCED occurrence of CANCER IN MICE.
What the REAL scientific results show is --------NO CONCLUSIVE RESULTS because the data of CANCER OCCURRENCE could be attributed to more than one VARIABLE.
WHEN WE READ A US NATIONAL FAKE MEDIA OR FAKE ACADEMIC ARTICLE WHICH SAYS------MAN-MADE GENE VECTORS SUCCESSFULLY REDUCED CANCER RATE IN MICE-----THAT IS FAKE NEWS----FAKE DATA.
What Are Transgenic Mice?
May 15, 2018| ingenious
| Mouse Models, Transgenic
What Are Transgenic Mice Used to Treat and Study?
What are transgenic mice and why have they become so popular in the past few years?
So many scientific papers feature the use of transgenic mice. A common strategy is to create a humanized line to study a particular human gene or disease. Once a new strain of humanized mice is developed, it can be used to understand debilitating diseases such as cancer, Parkinson’s, Alzheimer’s, diabetes, and more. However, there is far more than meets the eye, as specific transgenic mouse models are achieved more accurately than ever before with the help of advanced technologies like CRISPR/Cas9. What are transgenic mice really used for? The specifics relating to answering this question could fill entire volumes.
An Introduction to Transgenic Mouse Models
So let’s start at the beginning: what are transgenic mice?
The short answer is that they’re mice that have been artificially modified at a genetic level to include a foreign sequence, or transgene. This often involves the insertion of a human gene into the mouse’s genome to create a humanized mouse. The method for creating transgenic mice is versatile and it’s possible to create transgenic mice for many different kinds of research.
WE WILL BE DISCUSSING IN DETAIL WHY THESE 'HUMANIZED' MICE STUDIES ARE HIGHLY LIKELY FAKE NEWS.
Knockin vs. Transgenic Mice
Different methods for making mouse lines can create confusion when trying to understand “what are transgenic mice made for.” Generally, transgenic mouse models are created through random insertion of a gene, while the knockin models feature the introduction of the gene at a specific locus within the mouse genome. Creating models with the knockin strategy is more complex but removes the unpredictable element that comes with random transgenic insertion. Carefully evaluating the options along with your research plans is crucial to the long-term success of your lab’s research.
The Usefulness of the Transgenic Mouse for Research
A new transgenic mouse model generated by random insertion of foreign DNA may provide a boost to your current research. Compared with most models transgenic mice can be created at a relatively low cost and in a shorter amount of time.
If you’re studying a particular human gene for example you can investigate its function by making a transgenic model that expresses it in the mouse.
The Effective Generation of Specific Mouse Models
Over time as you continue to study the gene you may find that the random element that’s inherent in transgenic models becomes an obstacle. A common problem is that it’s better if the mouse gene is knocked out at the same time as the corresponding human gene is expressed. Since the transgene is inserted in a random location you’ll have to cross the new line with a knockout line and track two alleles throughout your research. A targeted knockin model can eliminate this by combining expression of the human sequence with knockout of the mouse sequence at a single genomic location. These advantages and others can make this model into a cornerstone of your research for years. However, if you’re focused on your immediate research objectives, a transgenic mouse may be the tool you need.
Today, research science in GENE VECTOR studies are leaving RANDOM INSERTION and trying to get that man-made gene vector to insert into VITAL DNA regions where very actively coded mice/human traits are located. Here's the problem:
These VITAL gene codes are HIGHLY SENSITIVE to changes in DNA structure-------in cell environmental chemistry. ANYTHING that throws a change-----simply removing ONE GENE------simply inserting ONE CODON -----will cause DNA replication to FAIL-------will cause ERROR in translation/transcription. There is NO WAY to tell in advance what those ERRORS-----what that ABORTED DNA translation/transcription will do to overall cellular process.
We are discussing ONE DNA STRAND replication ---------our cells have hundreds of DNA strands replicating all at the same time-------where these man-made gene vectors will insert is anybodies guess.
'One type of frameshift mutation is called an insertion. Just as the name implies, an insertion occurs when a single nitrogen base is accidentally added in the middle of the sequence. This throws off the reading frame of the DNA and the wrong amino acid is translated'.
Failure in these targeted gene insertions -----interfering with one single CODON ----one single CODON REGION----may not cause catastrophic results. A change in mice or human DNA -----a disrupted DNA translation may not harm/kill an animal.
The PROBLEM is when researchers DEREGULATE AREAS of DNA replication it is HIGHLY LIKELY that codons that are VITAL ----that codons that will harm or kill if CHANGED/DEREGULATED -----can and will occur.
Types and Examples of DNA Mutations
Mutations Happen When There Are Changes in the Nucleotide Sequence
by Heather Scoville THOUGHTCO.COM
Updated September 20, 2018
DNA mutations happen when there are changes in the nucleotide sequence that makes up the strand of DNA. This can be caused by random mistakes in DNA replication or even an environmental influence like UV rays or chemicals. The changes at the nucleotide level then influence the transcription and translation from gene to protein expression. Changing even just one nitrogen base in a sequence can change the amino acid that is expressed by that DNA codon which can lead to a completely different protein being expressed. These mutations range from being non-harmful all the way up to causing death.
A point mutation is usually the least harmful of the types of DNA mutations. It is the change of a single nitrogen base in a DNA sequence. Depending on the placement of that nitrogen base in the codon, it can cause no effect to the protein. Codons are a sequence of three nitrogen bases in a row that is "read" by messenger RNA during transcription and then that messenger RNA codon is translated into an amino acid that goes on to make a protein that will be expressed by the organism. Since there are only 20 amino acids and a total of 64 possible combinations of codons, some amino acids are coded for by more than one codon. Often, if the third nitrogen base in the codon is changed, it will not change the amino acid. This is called the wobble effect. If the point mutation occurs in the third nitrogen base in a codon, then it causes no effect on the amino acid or subsequent protein and the mutation does not change the organism.
At most, a point mutation will cause a single amino acid in a protein to change. While this usually is not a deadly mutation, it can cause issues with that protein's folding pattern and the tertiary and quaternary structures of the protein.
One example of a point mutation is sickle cell anemia. A point mutation caused a single nitrogen base in a codon for one amino acid in the protein called glutamic acid to instead code for the amino acid valine. This single small change causes a normally round red blood cell to instead be sickle-shaped.
Frame Shift Mutations
Frameshift mutations are much more serious and deadly than point mutations. Even though only one nitrogen base is affected just like in point mutations, this time the single base is either completely deleted or an extra one is inserted into the middle of a DNA sequence. This change in sequence causes the reading frame to shift, hence the name frameshift mutation.
A reading frame shift changes the three letter long codon sequence for messenger RNA to transcribe and translate. Not only is that amino acid changed, all subsequent amino acids are changed. This significantly changes the protein and can cause severe problems and even possibly death.
One type of frameshift mutation is called an insertion. Just as the name implies, an insertion occurs when a single nitrogen base is accidentally added in the middle of the sequence. This throws off the reading frame of the DNA and the wrong amino acid is translated. It also pushes the entire sequence down by one letter, changing all codons that come after the insertion and therefore completely altering the protein.
Even though inserting a nitrogen base makes the overall sequence longer, that does not necessarily mean the amino acid chain length will increase. In fact, it could seriously shorten the amino acid chain. If the insertion causes a shift in the codons to create a stop signal, a protein may never be made. Otherwise, an incorrect protein will be made. If the protein that has been changed was essential for life, then most likely the organism will die.
The other type of frameshift mutation is called a deletion. This happens when a nitrogen base is taken out of the sequence. Again, this causes the entire reading frame to change. It changes the codon and will also affect all amino acids that are coded for after the deletion. Nonsense and stop codons may also appear in the wrong places, much like an insertion.
DNA Mutation Analogy
Much like reading text, the DNA sequence is "read" by messenger RNA to produce a "story" or an amino acid chain that will be used to make a protein. Since each codon is 3 letters long, let's see what happens when a "mutation" occurs in a sentence that uses only three letter words.
THE RED CAT ATE THE RAT.
If there was a point mutation, the sentence would change to:
THC RED CAT ATE THE RAT.
The "e" in the word "the" mutated into the letter "c". While the first word in the sentence is no longer the same, the rest of the words still make sense and are what they are supposed to be.
If an insertion were to mutate the above sentence, then it might read:
THE CRE DCA TAT ETH ERA T.
The insertion of the letter "c" after the word "the" completely changes the rest of the sentence. Not only is the second word no longer readable, neither are any words after it. The entire sentence has changed into nonsense.
A deletion would do something similar to the sentence:
THE EDC ATA TET HER AT.
In the example above, the "r" that should have come after the word "the" has been deleted. Again, it changes the entire sentence. Even though in this example, some of the subsequent words are readable, the meaning of the sentence has completely changed. This shows that even if codons are changed into something that isn't nonsense, it still completely changes the protein into something that is no longer functional.
When genetic vector insertion research tells us DON'T WORRY---------this is very PRECISE--------it is very TARGETED-------
we say OH, REALLY???
Medical science these few decades was unable to be PRECISE with cancer treatments--------killing great sectors of NORMAL cells in trying to eliminate cancerous ones. We understand medical research is trying using bio-genetics to do just that. Find and administer treatment to individual cancerous cells to eliminate them. THAT is not bad research. This could lead to good basic science BUT the process targets CANCEROUS CELLS------with intervention NOT NORMAL cells or those normal cell's DNA replication process.
Each human cell as we described is very, very, very dependent on HOMEOSTASIS-----that means it REQUIRES the inside of a cell to remain UNCHANGED------because our NATURAL cell response to IMMUNITY will always react to any VECTOR entering a cell. NO PROBLEM says global banking 1%-----we will DEREGULATE that natural IMMUNE RESPONSE to see if man-made gene vectors can enter a cell just to be able to INSERT/DELETE these gene vectors.
So, this is the basic science happening over these few decades and today-------NO BASIC SCIENCE has been created in any of these studies EVEN IN MICE.
Report: U.S. drone strikes are less precise than claimed
A report from Amnesty International states that U.S. drone strikes in Pakistan are not as precise as American officials allege them to be, claiming that at least 19 civilians were killed in two drone strikes since January 2012, though the Obama administration maintains that the strikes are “increasingly accurate.”
Oct. 22, 2013 MSNBC ONLINE NEWS
NO SCIENTIFIC RESEARCH STUDY CAN CLAIM TO SUCCESSFULLY PROVE A HYPOTHESIS UNTIL THEY CAN CONTROL FOR VARIABLES -------BASIC SCIENCE HAS REACHED THOSE STANDARDS.
This is nowhere in site in MOVING FORWARD bio-genetic identification of disease vectors----treatment of disease vectors with DELETION/INSERTION of gene vector research.
Identifying the Strengths and Weaknesses of a Scientific Investigation for the GED Science Test
Identifying the Strengths and Weaknesses of a Scientific Investigation for the GED Science Test
The GED Science test will expect that you are able to identify strengths and weaknesses in a scientific investigation. Scientific investigations should be empirical; that is, conclusions should be based on verifiable observation, experience, and experimental evidence. For a scientific investigation to produce reliable results, it must meet all the following criteria:
- Participants/subjects must be chosen randomly.
- Controls must be in place to reduce or eliminate variables not being tested.
- Only one variable can be manipulated and tested. (More than one may be used, but that makes statistical analysis difficult.)
- Results must be quantifiable — size, number, weight, or something else that can be measured. For example, the number of hairs on a cat is quantifiable, although they would be very difficult to count, whereas the softness of the cat would be qualitative — a judgment call, unless you could figure out some way to quantify it.
- Participants/subjects must be assigned randomly to either the experimental or control group.
- Participants/subjects may also be retested, so they’re tested in both the experimental and the control group. This “repeated measure” technique produces more uniform results. When repeated measures are done, counterbalancing may also be done to reduce the effects of the order in which participants are tested in either the experimental or control group.
- All evidence must be reported, even if — and perhaps especially if — it doesn’t support the hypothesis. If evidence is excluded, the reason for the exclusion must be provided.
Controls are particularly important. When pharmaceutical companies conduct tests on medications, they commonly use the following three types of controls:
- Control group: A group that establishes a baseline from which results are measured. The control group receives no treatment or a neutral treatment. Results from the treated and untreated (control) groups are compared to determine whether treatment had any effect.
- Placebo: Untreated participants in a study often respond differently if they think they received treatment. To account for this placebo effect, researchers provide a neutral treatment (such as a “sugar pill”) that has no real effect.
- Blinding: Those conducting the study hide the fact that some participants are receiving a placebo and some aren’t, because when people know they’re getting a placebo, they’re less likely to respond to it. In a double-blind test, neither the researcher nor the participant is aware of who’s getting the placebo, so nobody involved can inadvertently influence the results by what they say or do.
We want to make one more reference to these two STEM research discussions detailing specific genetic vector research whether in SCIENTIFIC JOURNALS like NATURE-----or whether tons of global banking 1% FAKE SCIENCE NEWS/DATA journals and media.
The US separate from UK had its own scientific community ---we had plenty of US universities doing research which was PEER REVIEWED by our US 99% WE THE PEOPLE SCIENTISTS who were passionate to make sure SCIENTIFIC METHOD was used and RESULTS precise.
These few decades have eliminated all those US 99% WE THE PEOPLE SCIENTIFIC peer review and installed global corporate SCIENTISTS tied to LYING AND HIDING -----that's what they did in DARK AGES-----made sure those DARK AGE 99% of citizens had no idea what STEM advances were happening.
NATURE AND SCIENCE were the most respected in that regard--------but today even these UK OXFORD science journals released to public will tend to LIE AND HIDE. Not as much as global banking 1% FAKE NEWS AND DATA media and academic outlets.
Why do Scientists want to Publish in Nature or Science?
April 15, 2015 rishabhmjain
Academics have one primary currency, papers. Just like real currencies, the value of every paper is different, with a well-established high value placed on Nature, Science and similar high-impact journals. In this article I wanted to explore why publishing in these journals is so desirable to academics. More importantly, to ask the important question of whether these purposes can be solved in ways that are less expensive.
First of all, let’s establish the costs associated with publishing in Nature or Science:
- Time to do research:The burden is on the researcher to present a full and compelling story, this often implies that an enormous body of work is presented as a ‘single finding’ in one paper. If you read one of these articles however, it is clear that the authors are showing several independently important results, just presented as one to improve ‘impact.’ This is self-evident in the absurdly long supplemental information sections of a Nature or Science paper.
- Time in review:The average time a paper spends in review at a high impact journal is much longer than other journals, largely because reviewers are exceptionally critical and feel obliged to send a long list of comments, simply because the author submitted to a high impact journal. Also, higher impact journals will solicit more reviewers than medium impact journals, eg. Nature sends it to 2-4 as opposed to average of 2. Further, there are usually multiple rounds of review at these journals (again, much of which is inflated simply because of ‘journal ego’).
- Reviewer conflict of interest:Reviewers of high impact papers are always in a conflict of interest. The acceptance of a colleague’s paper in a high impact journal means that colleague is creating ‘high impact’ and ‘novel’ work in your field. This is a terrible conflict of interest where a researcher has to accept that someone else is producing ‘important’ work in their field, even if they are not. This is often a major indirect cost in these journals as it makes reviews highly biased and stretches ethics or academic integrity.
- Monetary cost:High impact journals, by virtue of being desirable also charge the most for publishing in their journals. This cost is borne directly by the authors despite the work not being made open access in general.
- Prestige / Perceived value: The sheer ability to publish work in one of these journals carries with it a perceived value by the scientific community that the research is ‘important’ and ‘good’ enough to get through the obscenely long and often unnecessary peer review process. However, this aspect of the benefit has to ‘real’ value. Meaning that the article does not ever have to help anyone or provide substantive value (eg. via citations) to have the researcher gain this perception benefit.
- Citation value: A major marketing benefit of a ‘high impact’ journal is that they carry a high Impact Factor. This simply means that the average number of citations per year for an article in that journal is high. However it does not mean that your article will be cited. In fact, journals have a very high skew, with few articles getting cited a lot and most articles getting cited very little. In Nature for example, the average number of citations for an article is 121 (over its life, till date). However, the median is 24 citations and over 40% of articles are cited less than 10 times! So if you submit to Nature, and you produce an ‘average’ Nature article, it will be cited 24 times-total!*
- Publicity value: The second major marketing advantage is that traditional and other mass media look to Science and Nature to publish flashy articles about cool new science. Given that Nature and Science are meant to be broad interest journals, this makes it very easy to get mass media to write about discoveries published in these journals. Further, the ‘news and views’ section in Nature journals makes it even more media friendly by getting top scientists to write their opinions of an article in that same issue – in lay words.
- Readership value: Building slightly on a point made in the previous section, these journals are broad. This means that scientists that have nothing to do with your field will still at least see your article (even if they don’t read it). This exposure benefit implies that there is a higher chance that your work will influence someone in some way that you didn’t expect, i.e. increase your real impact.
OK, so now that we have a pretty strong understanding of the various benefits a researcher obtains through publication in a high impact journal, we can elicit an important insight, that all of the benefits a high impact journal provides is on the marketing side of the paper.
Given that they are providing marketing value, the one advantage that is hard to reproduce or replace, is brand value. Our marketing friends at any major company will tell you that brand is hard to replace. However, it is certainly not impossible, especially given how easy it is to establish personal brands on the internet these days. In fact, several faculty have started doing this (check out this list!), using the internet to make themselves more discoverable, and have their personal brand push them forward rather than rely on Nature to do it for them.
The other benefits outlined above all boil down to a single insight, that high impact journals push articles to more eyes. It is pretty clear given the citation analysis above that your article must provide some substantive value for people to cite it, i.e. there are ‘duds’ even in Nature. So, to increase your citation count you simply need to get your article read by others. This implies 2 very simple actionable insights:
- You should write a lay version of your article, i.e. your own ‘news and views’ so that it is accessible to mass media and other fields
- You should promote your own content: either via 3rd party media outlets or direct
Thankfully, these are very easy to do. The internet has made accessible the ability to push or pull content to anyone in the world extremely easily. In fact, several faculty already do this in some form. I recently got forwarded an e-mail that was written by the author of a new paper directly to my Professor to advertise the paper (the paper was attached so we could read it too)! The list of actions one can take is quite large, but to get you started here are some:
- Direct e-mail to people you know are in your field: this is easy to find, just look at your citations to start!
- Writing a guest blog in a science blog: Check out scienceblogs.com
- Pushing your new article on social media: If professors don’t use social media, it doesn’t matter, grad students certainly do!
- Getting an article written by your university newspaper: I know MIT is really good about putting their research news on the front page of their website. Other universities do also get their faculties’ work pushed into the media!
So let’s return to the original question: ‘Why do Scientists want to Publish in Nature or Science?’ It looks to me like the value these journals provide can be replaced with lower cost alternatives. In fact, not only can scientists avoid the pain of trying to publish in these journals, they can do better by influencing directly the visibility and access to their work. The cherry that tops it off is that all of the content and marketing work they put in is owned by them and remains an asset of the scientist as opposed to that of Nature or Science. I am excited to see more and more scientists take ownership of their work, and build a stronger scientific ecosystem!
As always, let me know your thoughts in the comments section below. Specifically, if you have successfully marketed your work on your own, leave those ideas here for others to benefit from your insight!
*These statistics were calculated using the citation report generate by Thomson Reuters Web of Science.
Here is where all REAL LEFT SOCIAL PROGRESSIVE PUBLIC INTEREST regulation of medical research in US has been dismantled. The US used to REGULATE both CORPORATE R AND D-------and our university research departments with the goal of assuring no DAN BROWN'S INFERNO -------THE PROVOST and his MENDACIUM CORPORATION would hide and evade public oversight and accountability in PUBLIC SAFETY------PUBLIC INTEREST ---CRIMES AGAINST HUMANITY in scientific research------
YOU KNOW, ALL THAT HITLER ERA FASCIST MEDICAL EXPERIMENTATION THAT WAS INVESTIGATED IN INTERNATIONAL JUSTICE COURTS?
What is MOVING FORWARD today inside US FOREIGN ECONOMIC ZONES ------and has existed in overseas third world FOREIGN ECONOMIC ZONES these few decades of global banking 1% CLINTON/BUSH/OBAMA------is the installation of what an INTERNATIONAL JUSTICE COURT would call CRIMES AGAINST HUMANITY MEDICAL RESEARCH.
FORBES of course talking about PROGRESSIVE approval----meaning ECONOMIC PROGRESSIVE-------the OPPOSITE of LEFT SOCIAL PROGRESSIVE. Economic progressives place global corporate PROFITS ahead of HUMANITY.
This is what today is corrupting all of our strong US public interest---public health, welfare, and safety structures-------we need to STOP THIS FROM MOVING FORWARD.
Dec 14, 2016, 05:36pm
Trump's FDA Chief May Implement Progressive Approval For Drugs
Patrick Cox Contributor FORBES
President-elect Trump's cabinet appointments are generating a great deal of attention and controversy. After eight years of Democrat rule, it would be foolish to expect otherwise.
One appointment, though, will have a profound impact on your health… and the health of your loved ones.
The “progressive approval” process for drugs
The first potential FDA chief appointee leaked by the Trump transition team is Jim O’Neill. Managing director of Peter Thiel’s Mithril Capital, O’Neill has publicly supported proposals to do away with the FDA’s requirement for phase 2 and 3 trials. Instead, he favors “progressive approval” of drugs and other medical technologies.
THESE CLINICAL TRIAL REQUIREMENTS DISMANTLED THESE FEW DECADES OF CLINTON/BUSH/OBAMA----TRUMP SIMPLY MAKING IT OFFICIAL.
O’Neill would not be the first FDA head to favor progressive drug approval. Andrew von Eschenbach developed this system when he served as FDA chief. But during his tenure, Eschenbach was not able to put such a far-reaching reform into practice in the US.
The Japanese, though, saw the value of Eschenbach’s plan. They now use it for regenerative medicine. Japan legalizes therapies following proof of safety. Once a drug is in use, companies can move to phase 4. This means they monitor their patients and disclose efficacy data regularly.
If O’Neill gets the nod, he could implement progressive approval for drugs. But he would face fierce opposition from those who profit from the current system.
OH, REALLY?????? BUT ESCHENBACH IS THE CRIMINAL AND CORRUPT PROFITEERING STRUCTURE.
The current drug approval system is flawed
Big pharma benefits a great deal from the status quo. Since many small biotechs can’t fund most phase 2 or 3 trials, they give up significant ownership of their biotechnologies to these giants in exchange for financial help.
Many other organizations are also paid billions each year for services related to phase 2 and 3 clinical trials. They too will argue that doing away with those trials would endanger patients.
Since therapies would have to be proven safe before reaching the public, they will charge that patients will be at risk from using treatments that don’t work.
This, of course, is true. But it’s also true that patients are put at risk because they are denied access to unapproved but effective drugs.
Also, we pay much more for available drugs because companies must recoup costs imposed by the regulatory system. How big are those costs? Estimates of the average cost of one new medicine range from $1 to $4 billion.
Another side effect of the current system is that many drugs never leave the lab. These are drugs that could effectively treat serious illness but aren’t worth the cost of approval. This is because the patient population is too small to recoup approval costs.
The FDA has made efforts to help to help biotechs develop orphan drugs, but these steps have not been enough to make much of an impact.
Genomics and the need for a new regulatory process
Genomics has changed the way we treat illness. As the cost of genome sequencing falls, the ability to design drugs that work in small populations with specific genetic characteristics is rapidly increasing.
Eric Topol is the Director of the Scripps Translational Science Institute. He suggests that randomized clinical trials for this kind of indication are not just impractical, they’re unethical. InSilico Medicine’s Alex Zhavoronkov is one of the leading researchers in genomics-based personalized medicine. He believes we will be able to design and manufacture drugs for a single genome.
But how do you do a blinded controlled trial for a drug that may work on just one person?
This is not just an issue for the future. Many life-saving breakthroughs that could save millions of lives and reduce medical costs are stalled right now. Two of the most important areas of research are geroprotectors and induced tissue regeneration (ITR).
Geroprotectors are compounds that repair the systems that accelerate aging and age-related disease. Major universities and research organizations have found at least half a dozen molecules that could slow aging and extend health spans… even in older people.
Why haven’t you seen these compounds?
Because phase 2 and 3 trials would take a decade or more… while increasing their prices by orders of magnitude.
ITR is an emerging technology that could reactivate the embryonic healing powers hidden deep in your DNA. It could restore lost limbs, broken spinal cords, or any other body part to youthful function. Eyes, hearts, joints, skin, and livers could be taken back in time using relatively simple compounds.
If it weren’t for the fact that Dr. Michael West is spearheading this new field, I would dismiss it as a pipe dream. West’s spinal cord stem cell therapy recently saved complete quadriplegics from a life of total dependency. Almost no one thought that he could do this. In fact, I got emails saying that the trial would fail, and this was after the first patient got back to ability to lift weights, text, and care for himself.
The important thing to note about this therapy is how long it took to get approved. West invented it over 20 years ago. It took that long to drag this miraculous biotechnology through the regulatory maze.
The big picture for ITR
Over the past 20 years, the pace of West's research and scientific progress has accelerated along with breakthroughs in computers and genomics. Now, he is on the verge of activating in adults the same genetic power evident in developing embryos.
For years, I’ve gleaned what I could about this project by following West’s public statements and patent applications. Finally, he’s begun to tell the whole revolutionary story. Following the success of spinal cord technology, he laid out the big ITR picture in a keynote address to the prestigious World Stem Cell Summit.
ITR may be the biggest breakthrough in the history of medicine. The ability to make old and damaged organs and tissues young again will change countless lives. For millions of older people, though, it will come too late unless the regulatory bureaucracy is transformed to accelerate life-saving therapies.
Maybe Jim O’Neill will be the person to make it happen.
In the interest of transparency, I should note that I own stock in Michael West’s company BioTime (*see disclosure below).
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When REAL LEFT SOCIAL PROGRESSIVES shout these few decades of CLINTON/BUSH/OBAMA--that ALL of what came from atrocities during WW 2-----whether on the battle field ergo TREATMENT OF PRISONERS OF WAR-----or the atrocities of MEDICAL DR NO scientists who used war to escape the CIVIL SOCIETY structures against CRIMES AGAINST HUMANITY. Last century our global 99% and our Western nations embraced these protections of HUMANITY-------we built civil structures to assure these CRIMES AGAINST HUMANITY were not in our local communities.
Here in US we have a few cases identified as such-----but US history really has very few openly operating public health structures attacking citizens UNTIL RECENTLY. Our US mentally ill feel the bulk of this------these few decades of NOT READY FOR PRIME TIME PHARMA exposed our military troops and our US poor citizens to UNETHICAL medical exposures.
So, MOVING FORWARD back to 3000BC HINDI-BRAHMIN inside US FOREIGN ECONOMIC ZONES----will completely ERASE all of what has been WESTERN NATION CIVIL SOCIETY attitudes against CRIMES IN MEDICAL RESEARCH AND APPLICATIONS.
The US FDA has had appointed leaders to Federal HUMAN SAFETY agencies including HEALTH AND HUMAN SERVICES and FDA which swing for far-right global banking 1% and global corporations these few decades----so, it is not TRUMP MOVING FORWARD these medical research structures----it has been global banking 5% freemason/Greek player/pols black, white, and brown players.
SHAKE, SHAKE, SHAKE THOSE TAIL FEATHERS AND GET RID OF ALL GLOBAL BANKING 5% FREEMASON/GREEK PLAYERS WHO DON'T CARE.
We again remind------these policy stances in medical research are driven by both global banking 1% OLD WORLD KINGS KNIGHTS OF MALTA----AND TRIBE OF JUDAH--
Nuremberg war crimes trials 70 years on: a complex legacy
November 20, 2015 12.18am EST
On November 20 1945 the first of the Nuremberg trials began in the main court building of the Bavarian town of Nuremberg with the indictment of 22 of the most senior Nazis that had been captured alive.
Here in the dock were the architects and enforcers of the Holocaust and the Nazi regime’s countless other crimes – among them were Hermann Goering, head of the Luftwaffe and the Nazi rearmament effort; Hans Frank, who had treated Poland like his personal fiefdom and acquired the nickname “the Butcher of Kracow”; Hans Sauckel, who had organised the Nazi slave labour programme.
The trials are widely celebrated as a triumph of law over evil and marking an important turning point in legal history because dealing with the crimes of the Nazis paved the way for justice in the international community in general and the creation of the International Criminal Court in particular. It is this version of the story which has inspired the city of Nuremberg, which also hosted the infamous Nazi party rallies in the 1930s, to launch a new academy to promote the “Nuremberg principles”.
But while Nuremberg is celebrated today, the legal reality is not as clear-cut. As leading international criminal lawyer William Schabas remembers, “when I studied law, in the early 1980s, the Nuremberg Trial was more a curiosity than a model”.
The trials were also plagued by allegations of being little more than victor’s justice. These were made not only by Germans but also by American and British lawyers who felt it was a legal travesty. The judges and prosecutors were not neutral, but came from the four victorious powers – which led to such oddities as a Soviet prosecutor citing the Hitler-Stalin pact as evidence of German aggression against Poland, or a Soviet judge with ample experience of running Stalinist show trials trying to persuade his colleagues that the massacre against Polish officers in Katyn (who had been shot by the Soviets) should be added to the tally of German war crimes.
But the hypocrisy was not exclusive to the Soviet side: the London Charter of August 8 1945 which established the tribunal explicitly limited its remit to war crimes committed by the Axis powers. The tribunal also applied the so-called tu quoque principle which holds that any illegal act was justified if it had also been committed by the enemy (the Latin phrase means “you, too”).
No Nazi was charged with terror bombardment since the use of strategic bombardment against civilians had been a pillar of the British and US war efforts. And when US admiral Chester W. Nimitz testified that the US Navy had conducted a campaign of unrestrained submarine warfare against the Japanese from the day after Pearl Harbor, the relevant charges against Admiral Karl Doenitz were quietly dropped.
Wisely, the International Criminal Tribunal for the former Yugoslavia dismissed tu quoque as fundamentally flawed.
So why celebrate this trial?
One reason to celebrate Nuremberg is the simple fact that it happened at all. Until just before the end of the war, Churchill, Roosevelt and Stalin favoured summary executions of thousands of leading Nazis as the appropriate form of retribution. An outcry among the US public once these plans were leaked was a major factor in laying the road to Nuremberg.
Instead of mass shootings, an old idea from the First World War was revived. The Versailles treaty had compelled Germany to hand over Kaiser Wilhelm II and hundreds of senior officers to an international tribunal to be tried for war crimes. But the Kaiser fled to the Netherlands and the German government refused to hand over any officers or politicians. This time, however, Germany was completely occupied and was unable to resist, so the trials went ahead.
Flawed or not, the Nuremberg tribunal could not have met a more deserving collection of defendants – and it gave them a largely fair trial. Next to 12 death sentences and seven lengthy prison terms, the judgements included three acquittals – one of them for Hans Fritzsche, who had been the regime’s public voice on radio but was not personally involved in planning war crimes.
Crucially, the Nuremberg trials established an irrefutable and detailed record of the Nazi regime’s crimes such as the holocaust at precisely the time when many Germans were eager to forget or claim complete ignorance.
The legacy: important but inconvenient
Today, the most relevant legacy are the “Nuremberg principles”. Confirmed in a UN General Assembly resolution in 1948, they firmly established that individuals can be punished for crimes under international law. Perpetrators could no longer hide behind domestic legislation or the argument that they were merely carrying out orders.
The Nuremberg trials also influenced the Genocide Convention, the Universal Declaration of Human Rights and the Geneva conventions on the laws of war, all signed shortly after the war.